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Program

IIAS Research Conference 2011 on“Frontiers in Neuroscience: From Brain to Mind”PROGRAM- Tuesday, December 6 -14:00-15:00 Registration15:00-15:10 Opening RemarksKazuo Oike (IIAS)15:10-16:10 Opening LectureChair Person:Hitoshi Sakano (Univ. Tokyo)1. Deconstructing smellLinda Buck (Fred Hutchinson)16:30-18:30 Olfactory SystemChair Person:Lisa Stowers (Scripps)< Coffee Break >1. Molecular genetic dissection of olfactory neural circuitry in zebrafishYoshihiro Yoshihara (RIKEN)2. Evolution of olfactory receptor gene repertoires and functionSigrun Korsching (Univ. Cologne)18:30-20:30 Welcome Dinner- Wednesday, December 7 -9:30-12:30 Axons and WiringChair Person:Sigrun Korsching (Univ. Cologne)1. The neural circuitry of emotion in flies and miceDavid Anderson (Caltech)2. Wired for sex: the neurobiology of drosophila courtship behaviourBarry Dickson (IMP, Vienna)< Coffee Break >3. Kinesin superfamily molecular motors (KIFs) as key regulators for intracellular transport andhigher brain functionNobutaka Hirokawa (Univ. Tokyo)Short Talks12:30-13:30 Lunch13:30-17:00 SynapseChair Person:Nicholas Spitzer (UCSD)1. Signaling networks that regulate synapse development and cognitive functionMichael Greenberg (Harvard Univ.)2. Synaptic competition in the dendritic spines of CA1 pyramidal neuronsHaruo Kasai (Univ. Tokyo)< Coffee Break >3. Circuit mechanisms for perceptual memory of the temporal sequence and time intervals ofsensory eventsMu-ming Poo (UC Berkeley)Short Talks- Thursday, December 8 -9:30-12:30 Neural CircuitChair Person:Ivan Rodriguez (Univ. Geneva)1. Enhancement of activity and plasticity in visual cortexMichael Stryker (UCSF)2. Neuronal identity and circuit formation in the mouse olfactory systemHitoshi Sakano (Univ. Tokyo)< Coffee Break >3. Activity-dependent neurotransmitter respecification: novel plasticityNicholas Spitzer (UCSD)Short Talks12:30-13:30 Lunch13:30-17:00 Pheromone-induced BehaviorChair Person:Yoshihiro Yoshihara (RIKEN)1. Diverse coding logic to encode olfactory-mediated behaviorLisa Stowers (Scripps Inst.)2. Narrowly-tuned chemosensory reception for food and pheromone signalsKazushige Touhara (Univ. Tokyo)< Coffee Break >3. Emergence of novel chemosensors: from the immune to the olfactory systemIvan Rodriguez (Univ. Geneva)4. Calreticulin chaperones regulate functional expression of V2R pheromone receptorsHiroaki Matsunami (Duke Univ.)17:00-18:30 Poster Presentation18:30-20:30 Dinner6 7

- Friday, December 9 -9:30-12:30 Sensory PerceptionChair Person:Hiroaki Matsunami (Duke Univ.)1. Genes that are selectively expressed in regions of primate neocortex: the functions andimplication for cortical specializationTetsuo Yamamori (NIBB)2. Olfactory white: odorant mixtures containing many components converge towards a commonperceptNoam Sobel (Weizmann Inst.)< Coffee Break >12:30-13:30 Lunch3. Toward the circuit physiology of midbrain dopamine neurons: beyond stamp collectingNaoshige Uchida (Harvard Univ.)4. Sensory experience-dependent reorganization of neuronal circuits in the olfactory cortex andolfactory bulb during postprandial sleepKensaku Mori (Univ. Tokyo)Invited Speakers13:30-16:30 Cognition and BehaviorChair Person:Tetsuo Yamamori (NIBB)1. A neandertal perspective on human originsSvante Pääbo (Max Planck)2. Functional architecture of cerebral cortexKenichi Ohki (Kyushu Univ.)< Coffee Break >3. Functional division among prefrontal areas in macaque monkeysKeiji Tanaka (RIKEN)4. Cognitive development in humans and chimpanzeesTetsuro Matsuzawa (Kyoto Univ.)16:30-17:30 Closing LectureChair Person:Sigrun Korsching (Univ. Cologne)1. Experimental and theoretical approaches to conscious processingJean-Pierre Changeux (Collège de France)17:30-17:35 Concluding RemarksYoshiro Shimura (IIAS)8

Invited SpeakersThe neural circuitry of emotion in flies and miceThe neural circuitry of emotion in flies and miceDavid AndersonCalifornia Institute of TechnologyDavid AndersonCalifornia Institute of TechnologyResearch interests in my laboratory focuses on understanding how emotionalbehavior is encoded in the brain, at the level of specific neuronal circuits, and thespecific neuronal subtypes that comprise them. We want to understand thestructure and dynamic properties of these circuits and how they give rise to theoutward behavioral expressions of emotions such as fear, anxiety or anger. Thisinformation will provide a framework for understanding how and where in thebrain emotions are influenced by genetic variation and environmental influence(“nature” and “nurture”), and the mechanism of action of drugs used to treatpsychiatric disorders such as depression. We are using both mice and thevinegar fly Drosophila melanogaster as model systems. A central focus of thelaboratory is on the neural circuits underlying aggression and fear. We are usingmolecular genetic tools, as well as functional imaging and electrophysiology, toestablish cause-and-effect relationships between the activity of specific neuronalcircuits and behavior. We hope that this research will lead to new insights into theorganization of emotion circuits, and their dysregulation in psychiatric disorders.NAME:BUSINESS ADDRESS:DAVID JEFFREY ANDERSON, PH.D.California Institute of Technology1200 E. California Blvd.Division of Biology, 216-76Pasadena, CA 91125EDUCATION1978 A.B. Biochemical Sciences; Harvard College (advisor: D. ranton)1983 Ph.D. Cell Biology; Rockefeller University (advisor: G. Blobel)1986 Postdoctoral Molecular Biology; Columbia University,College of Physicians and Surgeons (advisor: R. Axel)ACADEMIC APPOINTMENTS2009 Seymour Benzer Professor of Biology,California Institute of Technology2004- 2009 Roger W. Sperry Professor of Biology,California Institute of Technology1996- 2004 Professor of Biology, California Institute of Technology1996- present Investigator, Howard Hughes Medical Institute1992- 1996 Associate Professor of Biology (tenured),California Institute of Technology1992-1996 Associate Investigator, Howard Hughes Medical Institute1989- present Adjunct Assistant Professor of Cell and Neurobiology,USC School of Medicine 101989-1992 Assistant Investigator, Howard Hughes Medical Institute1986-1992 Assistant Professor of Biology,1996- 2004 Professor of Biology, California Institute of Technology1996- present Investigator, Howard Hughes Medical Institute1992- 1996 Associate Professor of Biology (tenured),California Institute of Technology1992-1996 Associate Investigator, Howard Hughes Medical Institute1989- present Adjunct Assistant Professor of Cell and Neurobiology,USC School of Medicine1989-1992 Assistant Investigator, Howard Hughes Medical Institute1986-1992 Assistant Professor of Biology,California Institute of TechnologyAWARDS AND HONORS2011 Harvey Lecture, Rockefeller2011 Seymour Benzer Lecture, Oberlin College2011 Kuffler Lecture, Harvard Medical School2010 Allen Distinguished Investigator2010 Max Birnstiel Lecture, IMP, Vienna2009 Honors Lecture, NYU School of Medicine2008 Picower Lecture, MIT2007 Elected Member, National Academy of Sciences2005 Alexander von Humboldt Award2004 Named Roger W. Sperry Professor of Biology, California Institute ofTechnology2004 NYU School of Medicine Honors Lecture, Speaker2004 Learning and Memory Picower Lecture, MIT2004 The Joseph L. Melnick distinguished Guest Lecturer, BaylorCollege of Medicine2003 Keynote Speaker, Gordon Conference on Angiogenesis2003 Keynote Speaker, Gordon Conference on Neurotrophins2002 American Association for the Advancement of Science Fellow2002 American Academy of Arts and Sciences Fellow2001 Swirling Lecture, Harvard University2001 Elected Associate, The Neurosciences Institute2001 Mager Lecture, Hebrew University, Jerusalem2000 Visiting Professor, College de France1999 Alden Spencer Award in Neurobiology, Columbia University1998 Ferguson Award for Graduate Teaching1996 Ferguson Award for Biology Education2001 Ferguson Award for Graduate Teaching1993 Donald D. Matson Lecture, Harvard University1990 Charles Judson Herrick Award in Comparative Neurology1989 Javits Investigator in Neuroscience (NIH)1988 Pew Faculty Fellowship for Neuroscience Research1988 Alfred P. Sloan Research Fellowship in Neuroscience1987 Searle Scholars Award1986 NSF Presidential Young Investigator Award1983-86 Helen Hay Whitney Foundation Fellow1978 NSF Predoctoral Fellow1978 A.B. Summa Cum Laude, Harvard College, Phi Beta KappaAWARD SELECTION COMMITTEES2004 -2008 McKnight Neuroscience of Brain Disorders Awards SelectionCommittee2002-2007 Alfred P. Sloan Research Fellowships in NeuroscienceProgram Committee2001-present Wiley Prize Selection Committee1996 Sloan General Motors Cancer Research Award,Vice-Chair, Selection 11 Committee1995 Sloan Prize, General Motors Cancer Research FoundationSelection Committee

2004 -2008 McKnight Neuroscience of Brain Disorders Awards SelectionCommittee2002-2007 Alfred P. Sloan Research Fellowships in NeuroscienceProgram Committee2001-presentWiley Prize Selection Committee1996 Sloan General Motors Cancer Research Award,Vice-Chair, Selection Committee1995 Sloan Prize, General Motors Cancer Research FoundationSelection CommitteePROFESSIONAL ACTIVITIES2011 Neural Coding Advisory Council, Allen Institute for BrainScience2010- present Neural Systems & Circuits Editorial Board2010- present Connectional Atlas Advisory Council, Allen Institute for BrainScience2009- present SAB Chair, Allen Institute for Brain Science SAB2009- present Scientific Advisory Committee, Helen Hay WhitneyFoundation2007- 2009 Scientific Center Advisory Council, Allen Institute for BrainScience2006- 2009 SAB Member, Autism Consortium2007- 2009 SAB Member, Allen Institute for Brain Science2002- 2008 SAB Member, Allen Institute Brain Atlas2002- present The International Behavioural and Neural Genetics Society2002- 2006 Gene Expression International Journal of Cellular andMolecular Science Editorial Board2001- present SAB Member, Vascular Biology Institute Board2001- 2006 Board of Directors, International Society for Stem CellResearch2001 Hereditary Disease Foundation Scientific Advisory Board1999- present Journal of Regenerative Medicine Editorial Board1998- 2002 Annual Reviews Editorial Board1997- present SAB Member, Stem Cells, Inc.1995- present Development Editorial Board1995- present Molecular and Cellular Neuroscience Editorial Board1991- present American Association for the Advancement of Science1990- present Society for Developmental Biology1990- present Society for Neuroscience1989- present Neuron Editorial Board1989- 2000 Cambridge Neuroscience Scientific Advisory Board1991-1997 J. Neuroscience Editorial Board1995-1997 Developmental Biology Editorial Board1995-1997 American Society for Cell Biology1996-1997 CIT Presidential Search Committee MemberSCIENCE COMMUNITY SERVICE2010 Panel Member on PBS Charlie Rose program "The Anxious Brain"2010 Natural History Museum of Los Angeles, "First Fridays"presentation series2004 California Science Center National Fear Exhibit Technical AdvisoryBoard2004 The California Stem Cell Research & Cures Act Speakers’ Bureau2003 Californians for Stem Cell Research & Cures Scientific AdvisoryCouncil Co-Chair2002 CuresNow Scientific Advisory Board2003 Californians for Stem Cell Research & Cures Scientific AdvisoryCouncil Co-Chair2002 CuresNow Scientific Advisory BoardRECENT PUBLICATIONSHochstim, C.J. Deneen, B., Lukaszewicz, A., Zhou, Q., and Anderson, D.J.(2008) Identification of positionally distinct astrocyte subtypes whose identitiesare specified by a homeodomain code. Cell 133(3):510-22. PMCID:PMC2394859Wang, L. and Anderson, D. J. (2008) A common genetic target for environmentaland heritable influences on aggressiveness in Drosophila. PNAS15;105(15):5657-63. PMCID: PMC2311352Cell. 2009 Dec 24;139(7):1353-65. Epub 2009 Dec 10.Sensory neuron-specific GPCR Mrgprs are itch receptors mediating chloroquineinducedpruritus.Liu Q, Tang Z, Surdenikova L, Kim S, Patel KN, Kim A, Ru F, Guan Y, Weng HJ,Geng Y, Undem BJ, Kollarik M, Chen ZF, Anderson DJ, Dong X.Lebestky, T., Chang, J., Dankert, H., Zelnik, L., Kim, Y., Han, K., Perona, P., andAnderson, D.J. (2009) Genetically Separable Circuits Mediating Distinct Formsof Arousal are Oppositely Regulated by the D1 Receptor Ortholog DopR inDrosophila. Neuron 64(4)522-36. PMCID: PMC2908595Yorozu, S., Wong, A., Fischer, B.J., Dankert, H., Kernan, M.J., Kamikouchi, A.,Ito, K., and Anderson, D.J. (2009) Distinct sensory representations of wind andnear-field sound in the Drosophila Brain. Nature 458:201-5PMCID:PMC2755041Dankert, H., Wang, L., Hoopfer, E.D., Anderson, D.J., and Perona, P. (2009)Automated Monitoring and Analysis of Social Behavior in Drosophila. NatureMethods EPub March 8 2009: 4:297-303 PMCID:PMC2678418Wang, L., and Anderson, D.J. (2010) Identification of an agression-promotingpheromone and its receptor neurons in drosophila. Nature 463(7278):227-31.PMID: 19966787. PMC2999963Haubensak, W., Kunwar, P.S., Cai, H., Ciocchi, S., Wall, N.R., Ponnusamy, R.,Biag, J., Dong, H-W., Deisseroth, K., Callaway, E.M., Fanselow, M.S., L・hi, A.,and Anderson, D.J. (2010) Genetic Dissection of an Amygdala Microcircuit thatGates Conditioned Fear. Nature 468(7321):270-76 NIHMS243118. [PubMed - inprocess]Lin, D., Boyle, M.P., Dollar, P., Lee, H., R., Perona, P., Lien, E.S., and Anderson,D.J. (2011) Functional identification of an aggression locus in the mousehypothalamus. Nature 470(7333):179-81 [PubMed - in process]Wang, L., Han, X., Mehren, J., Hiroi, M., Billeter, J-C., Miyamoto, T., Amrein, H.,Levine, J.D., and Anderson, D.J. (2011) Hierarchical chemosensory regulation ofmale-male social interactions in Drosophila . Nature NeuroscienceJune;14(6):757-62. Epub 2011 Apr 24. PMID: 21516101 [PubMed - in process]RECENT PUBLICATIONS12 13Hochstim, C.J. Deneen, B., Lukaszewicz, A., Zhou, Q., and Anderson, D.J.(2008) Identification of positionally distinct astrocyte subtypes whose identities

Deconstructing smellDeconstructing smellLinda B. BuckHoward Hughes Medical InstituteFred Hutchinson Cancer Research CenterInvited SpeakersLinda B. BuckHoward Hughes Medical InstituteFred Hutchinson Cancer Research CenterThe sense of smell allows humans and other mammals to detect a multitude ofenvironmental chemicals. Most are perceived as odors, but some, such as pheromonesand predator odors, elicit hormonal changes or instinctive behaviors. In early work, wediscovered the odorant receptor (OR) family, which mediates odor detection in the nasalolfactory epithelium (OE). Our studies showed that ORs are used in a combinatorialfashion to detect odorants and encode their unique identities, a scheme explaining hownearly identical chemicals can be distinguished. We found that each OE neuronexpresses a single OR gene and that while thousands of neurons with the same OR arescattered in one OE zone, they all synapse in a few specific glomeruli at semistereotypedlocations in the olfactory bulb. The spatial code for an odorant in the noseis thus a dispersed ensemble of neurons expressing different OR components of thechemical's receptor code whereas in the olfactory bulb it is a specific combination ofglomeruli whose arrangement is similar among individuals. In other studies, we andothers uncovered three different families of chemosensory receptors in the vomeronasalorgan (VNO), which is involved in pheromone detection. To study neural circuitsunderlying odor and pheromone sensing, we are employing genetic transneuronaltracers. By examining the connections of hypothalamic neurons that controlreproduction, we obtained evidence that those neurons are likely to obtain pheromonesignals from the OE as well as the VNO. In a subsequent search for potentialpheromone receptors in the OE, we discovered a second small family of OE receptors,called TAARs. At least two TAARs detect compounds elevated in male versus femalemouse urine, suggesting that TAARs may be involved in the detection of social cues.NAME:ADDRESS:PLACE OF BIRTH:Linda B. BuckEDUCATION AND TRAINING:Fred Hutchinson Cancer Research CenterDivision of Basic Sciences, A3-0201100 Fairview Avenue NorthSeattle, WA 98109-1024http://labs.fhcrc.org/buck/index.htmlSeattle, Washington1975 B.S. Microbiology, University of Washington, Seattle, Washington1975 B.S. Psychology, University of Washington, Seattle, Washington1980 Ph.D. Immunology, Microbiology Department, University of Texas SouthwesternMedical Center, Dallas, Texas, Advisor: Ellen Vitetta1980-82 Postdoctoral Fellow, Microbiology Department, Columbia UniversityCollege of Physicians and Surgeons, New York, New York, Laboratory ofBenvenuto Pernis1982-84 Postdoctoral Fellow, Institute of Cancer Research, Columbia UniversityCollege of Physicians and Surgeons, New York, New York, Laboratory ofRichard Axel1984-91 Associate, Howard Hughes Medical Institute, Columbia University Collegeof Physicians and Surgeons, New York, New York, Laboratory of RichardAxelACADEMIC APPOINTMENTS:1991-1996 Assistant Professor, Department of Neurobiology, Harvard MedicalSchool, Boston, Massachusetts1994-1997 Assistant Investigator, Howard Hughes Medical Institute1996-2001 Associate Professor, Department of Neurobiology, Harvard MedicalSchool, Boston, Massachusetts1997-2001 Associate Investigator, Howard Hughes Medical Institute2001-2002 Professor, Department of Neurobiology, Harvard Medical School, Boston,Massachusetts2001- Investigator, Howard Hughes Medical Institute2002- Full Member, Division of Basic Sciences, Fred Hutchinson CancerResearch Center, Seattle, Washington1415

2003- Affiliate Professor, Department of Physiology and Biophysics, Universityof Washington, Seattle, Washington2004-2007 Associate Director, Division of Basic Sciences, Fred Hutchinson CancerResearch Center, Seattle, WashingtonOTHER APPOINTMENTS:1997- Editorial Board, Current Opinion in Neurobiology2000-2003 Scientific Advisor, Primal, Inc., Seattle, WA2002- Editorial Board, Molecular and Cellular Neuroscience2003- Editorial Board, Developmental Neurobiology2003-2006 Scientific Advisory Board, Nura Inc., Seattle, WA2004- Scientific Advisory Board, Center for Molecular Medicine, KarolinskaHospital, Stockholm, Sweden2005- Medical Advisory Board, The Gairdner Foundation, Toronto, Canada2005- Advisory Committee, March of Dimes Prize in Developmental Biology2005- President's Council, New York Academy of Sciences2005- Editorial Advisory Council, HFSP Journal2005-2009 Advisory Board, Peter Gruber Foundation Neuroscience Prize2006- Founding Board, Rosalind Franklin Society2007- Consultant, Omeros Corp., Seattle, WA2007- Board of Directors, International Flavors & Fragrances, Inc., New York2007 Member, Kavli Prize Committee in Neuroscience2007 Committee Member, Unilever Science Prize2008 Committee Member, Kavli Prize in Neuroscience2009 Committee Member, The Royal Swedish Academy of Sciences GöranGustafsson Prize2010- Committee Member, Shaw Prize in Life Science and Medicine2011 Committee Member, Eric Kandel Young Neuroscientists Prize, The HertieFoundationSELECTED HONORS AND AWARDS:1992 The Takasago Award for Research in Olfaction1992 The LVMH Moet Hennessy Louis Vuitton Science for Art Prize1992 The Sense of Smell Award, The Fragrance Foundation1992 McKnight Scholar Award from The McKnight Endowment Fund forNeuroscience1992 Alfred P. Sloan Research Fellowship Award1993 John Merck Scholarship in the Biology of Developmental Disabilities inChildren1995 The 1995 Distinguished Alumnus, Graduate School, University of TexasSouthwestern Medical Center1996 The Unilever Science Award1996 The R.H. Wright Award in Olfactory Research1997 The Lewis S. Rosenstiel Award for Distinguished Work in Basic MedicalResearch2000 Senior Scholar Award in Aging, The Ellison Medical Foundation2002 Fellow, the American Association for the Advancement of Science2003 Member, the National Academy of Sciences2003 Perl/UNC Neuroscience Prize2003 The Gairdner Foundation International Award2004 The Nobel Prize in Physiology or Medicine2005 Golden Plate Award, The Academy of Achievement2005 Distinguished Alumnus Award, University of Washington2005 Brava Award, Women's University Club2006 The International Hall of Fame, International Women's Forum2006 Alumna Summa Laude Dignata, University of Washington2006 Member, the Institute of Medicine of the National Academies16 17

2006 Alumna Summa Laude Dignata, University of Washington2006 Member, the Institute of Medicine of the National Academies2007 The Medal of Merit, State of Washington2008 Member, the American Academy of Arts & Sciences2009 Member, the European Academy of SciencesBIBLIOGRAPHY (selected):Buck L and Axel R (1991) A novel multigene family may encode odorant receptors: aa molecular basis basis for for odor odor recognition. Cell Cell 65:175-187.Ressler KJ, Sullivan SL and Buck LB (1993) A zonal organization of odorant receptor geneexpression in the olfactory epithelium. Cell 73:597-609.Ressler KJ, Sullivan SL, and Buck LB (1994) Information coding in the olfactory system:evidence for a stereotyped and highly organized epitope map in the olfactory bulb. Cell79:1245-1255.Sullivan SL, Bohm S, Ressler KJ, Horowitz LF and Buck LB (1995) Target-independentpattern specification in the olfactory epithelium. Neuron 15:779-789.Malnic B, Godfrey PA, and Buck LB (2004) The human olfactory receptor gene family.Proc. Natl. Acad. Sci. USA. 101:2584-2589.Boehm U, Zou Z, Buck LB (2005) Feedback loops link odor and pheromone signaling withreproduction. Cell 123(4):683-95.Liberles SD, Buck LB (2006) A second class of chemosensory receptors in the olfactoryepithelium. Nature 442:645-650.Petrascheck M, Ye X, and Buck LB (2007) An antidepressant that extends lifespan in adultCaenorhabditis elegans. Nature 450-553-556.Liberles SD, Horowitz LF, Kuang D, Contos JJ, Wilson KL, Siltberg-Liberles J, Liberles DA,Buck LB (2009) Formyl peptide receptors are candidate chemosensory receptors in thevomeronasal organ. Proc. Natl. Acad. Sci. USA. 106:9842-9847.Nara K, Saraiva LR, Ye X, Buck LB (2011) A large-scale analysis of odor coding in theolfactory epithelium. J. Neurosci. 31:9179-9191.Sullivan SL, Adamson MA, Ressler KJ, Kozak CA and Buck LB (1996) The chromosomaldistribution of mouse odorant receptor genes. Proc. Natl. Acad. Sci. USA 93:884-888.Berghard A, Buck LB, and Liman ER (1996) Evidence for distinct signaling mechanisms intwo mammalian olfactory sense organs. Proc. Natl. Acad. Sci. USA 93:2365-2369.Berghard A and Buck LB (1996) Sensory transduction in vomeronasal neurons: evidencefor G Gao, , Gai2, G , and adenylyl cyclase II II as major components of of a pheromone signalingcascade. J. Neurosci. 16:909-918.Matsunami H and Buck LB (1997) A multigene family encoding a diverse array of putativepheromone receptors in mammals. Cell 90: 775-784.Malnic B, Hirono J, Sato T and Buck LB (1999) Combinatorial receptor codes for odors.Cell 96: 713-723.Horowitz LF, Montmayeur J, Echelard Y and Buck LB (1999) A genetic approach to traceneural circuits. Proc. Natl. Acad. Sci. USA 96:3194-3199.Matsunami H, Montmayeur J-P and Buck LB (2000) A family of candidate taste receptorsin human and mouse. Nature 404: 601-604.Montmayeur J-P, Liberles SD, Matsunami H and Buck LB (2001) A candidate tastereceptor gene near a sweet taste locus. Nature Neurosci. 4:492-498.Sam M, Vora S, Malnic B, Ma W, Novotny MV and Buck LB (2001) Odorants may arouseinstinctive behaviours. Nature 412: 142.Godfrey PA, Malnic B, and Buck, LB (2004) 4 The mouse olfactory receptor gene family.Proc. Natl. Acad. Sci. USA. 101:2156-2161.18 19

Invited SpeakersExperimental and theoretical approachesto conscious processingExperimental and theoretical approaches to consciousprocessingJean Pierre ChangeuxCollège de FranceJean Pierre ChangeuxCollège de FranceThe presentation focuses on the well-delimited issue of how an external or internalpiece of information gains access to conscious processing, as characterized by areportable subjective experience. Converging neuroimaging and neurophysiologicaldata, acquired during conscious and nonconscious processing, point to objectiveneural measures of conscious access: late amplification of relevant sensory activity,long-distance cortico-cortical synchronization at beta and gamma frequencies, and‘‘ignition’’ of a large-scale prefronto-parietal network. These findings are comparedto current theoretical models of conscious processing, including the Global NeuronalWorkspace (GNW) model according to which conscious access occurs when incominginformation is made globally available to multiple brain systems through a networkof neurons with long-range axons densely distributed in prefrontal,parieto-temporal, and cingulate cortices. The clinical implications of these resultsfor general anesthesia, coma, vegetative state, and schizophrenia are discussed.1) Academic trainingEcole Normale Supérieure (rue d'Ulm, Paris) (1955) and Licence de SciencesNaturelles (1956, 1957) at Paris University.Diplôme d'Etudes Supérieures (Mention Très Bien et Félicitations duJury) (1958).Agrégé des Sciences Naturelles (received first) (1958). Doctorat d'Etat de SciencesNaturelles, Paris (Mention Très Honorable et Félicitations du Jury), under thesupervision of Pr. Jacques Monod, Institut Pasteur (1964).2) Academic positionsAgrégé-préparateur of Zoology, Ecole Normale Supérieure, 1958 ; Postdoctoranlfellow, Universiy of California, Berkeley, 1965-1966 ; visiting Assistant ProfessorColumbia University College of Physicians & Surgeons, New-York, 1966-1967 ;Sous-Directeur, Collège de France, Paris (Chaire de Biologie Moléculaire), 1967 ;Director of the Unit of Molecular Neurobiology, Institut Pasteur, Paris, 1972-2006 ;Professor Collège de France, 1975-2006 ; Professor Institut Pasteur, 1975-2006,emeritus since 2007 ; Skaggs distinguished visiting professor in Pharmacology,University of California San Diego 2008-2011.3) Scientific prizes and awardsPrix Alexandre Joannidès, Académie des Sciences, Paris, 1977 ; GairdnerFoundation Award, Toronto, Canada, 1978 ; Richard Lounsbery Prize, NationalAcademy of Sciences, Washington (USA) and Académie des Sciences, Paris, 1983 ;Wolf Foundation Prize in Medicine, Jerusalem, Israel, 1983 ; Prix Broquette-Gonin,Académie Française, for l'"Homme Neuronal", 1983 ; Ciba Geigy Drew Award inBiomedical Research, Madison, 1985 ; F.O. Schmitt medal and prize, NeuroscienceResearch Program, Rockefeller University, New York, 1986 ; Rita Levi-MontalciniAward, Fidia Research Foundation, Washington, 1988 ; Bristol-Myers-SquibbAward in Neuroscience, New York, 1990 ; Carl-Gustaf Bernhard medal, SwedishRoyal Academy of Sciences, Stockholm, 1991 ; Science for Art, Prix d'HonneurLVMH, Paris, 1992 ; International Prize Amedeo e Frances Herlitzka forPhysiological Sciences, Torino, 1992 ; Médaille d'Or, Centre National de laRecherche Scientifique, Paris, 1992 ; Louis Jeantet Prize for Medicine, Geneva,1993 ; Thudichum medal, Biochemical Society, London 1993 ; Goodman and GilmanAward in drug receptor pharmacology, American Society for Pharmacology andExperimental Therapeutics, Anaheim, California, 1994 ; Camillo Golgi medal,Accademia Nazionale dei Lincei, Rome 1994 ; Sir Hans Krebs medal, FEBS,Helsinki, 1994 ; Max-Delbrück medal, in Molecular Medicine, Berlin, 1996; GrandPrix de la Fondation pour la Recherche Médicale, Paris, 1997 ; Jean-Louis Signoretprize in Neuropsychology, Paris, 1997 ; Emanuel Merck prize in Chemistry,Darmstadt, 1998 ; Linus Pauling medal, 1998/1999, Stanford, USA ; Eli Lilly awardin preclinical Neuroscience, European College of Neuropsychopharmacology,London, 1999 ; Langley Award for basic research on nicotine and tobacco,Washington, 2000 ; Balzan Prize for Cognitive Neuroscience, Berne, 2001 ;American Philosophical Society’s Karl Spencer Lashley Award in neuroscience,Philadelphia, 2002 ; Lewis Thomas Prize for Writing about Science, RockefellerUniversity, New-York, 2005 ; Dart/NYU Biotechnology Award in BasicBiotechnology, New- York, 2006 ; Golden Eurydice Award from InternationalForum of Biophilosophy, Bruxelles, 2006 ; National Academy of Sciences Award inthe Neurosciences, Washington, 2007 ; Neuronal plasticity prize, IPSENFoundation, Geneva, 2008 ; International College of NeuroPsychopharmacologyPioneer Award, for the fundamental discoveries concerning « The structure andfunction of the nicotinic acetylcholine receptor», Munchen, 2008 ; Passarow awardfor «extraordinary achievements in neuropsychiatric research», Los Angeles, 2010.4) Academies & Honorary degreesDeutsche Akademie der Naturforscher Leopoldina zu Halle (Pharmacology), 1974 ;Académie deMédecine de Turin, 1976 ; National Academy of Sciences, Washington(USA) (foreign associate), 1983 ; Royal Academy of Sciences, Stockholm, (Sweden)(foreign member), 1985 ; Académie des Sciences, Paris, 1988 ; Académie Royale deMédecine de Belgique (Bruxelles) (foreign honorary member), 1988 ; AcademiaEuropaea (founding member), 1988 ; American Academy of Arts and Sciences,Boston, (USA) (foreign member), 1994 ; Romanian Academy of Medical Sciences,Bucarest (foreign member), 1996 ; Institute of Medicine of the National Academies,Washington, (USA) (foreign associate), 2000 ; Istituto Veneto di Scienze, Lettere EdArti, Venezia (Italy), 2001 ; Hungarian Academy of Sciences, Budapest (foreignmember associate), 2004 ; European Academy of Sciences, Bruxelles (member),2004 ; International Academy of Humanism ; Académie Royale des Sciences, desLettres & des Beaux-Arts de Belgique (foreign member), 2010; AccademiaNazionale dei Lincei, Rome, (Italy) (foreign member) , 2010. Doctor honoris causa :Universities of Torino, Italy, 1989 ; Dundee, Scotland, 1992 ; Geneva, Switzerland,1994 ; Stockholm, Sweden, 1994 ; Liège, Belgium, 1996 ; Ecole PolytechniqueFédérale of Lausanne, Switzerland, 1996 ; University of Southern California, LosAngeles, USA, 1997 ; Bath, UK, 1997 ; Montréal University, Canada, 2000 ; TheHebrew University of Jerusalem, Israel, 2004 ; Ohio State University, Columbus,USA, 2007 ; University of Buenos Aires, Argentina, 2010.2021

5) Honorary conferences (selection)Smith, Kline and French Lectures in Pharmacology, Vanderbilt University, Schoolof Medicine (USA), 1974; Third Louis B. Flexner Lecture, University ofPennsylvania, Philadelphia (USA), 1974 ; Fourth FEBS Ferdinand SpringerLecture, 1975 ; William Draper Harkins Memorial Lecture, Department ofChemistry, University of Chicago (USA), 1977 ; Windsor C. Cutting MemorialLecture, Department of Pharmacology, Stanford University (USA), 1978 ; JohnKrantz Memorial Lecture, Department of Pharmacology, Baltimore (USA), 1978 ;Harvey Lecture, Rockfeller University, New York (USA), 1980 ; Wolfgang PauliVorlesungen Lecture, E.T.H. Zurich (Switzerland), 1980 ; Otto Loewi MemorialLecture, Department of Pharmacology, New York University (USA), 1982 ;Conférence Pfizer, Institut de Recherches Cliniques de Montréal (Canada), 1985;Woodward Lecture, Yale University, 1985 ; Wittaker Distinguished Lecture inBrain Science, Massachusetts Institute of Technology, Cambridge, MA. (USA),1986 ; First Walter Dandy lecture, Baltimore (USA), 1986 ; Warner-LambertLecture, 17th Annual Meeting of the Society for Neuroscience, New Orleans (USA),1987 ; First Trends in Pharmacological Sciences Lecture, FASEB meeting,Washington (USA), 1990 ; Aharon Katzir-Katchalsky Lectures, Rehovot (Israel)1990 ; Third Jean Brachet Memorial Lecture, Bruxelles (Belgium), 1991 ; Openinglecture European Neuroscience Association meeting, Cambridge (U.K.), 1991 ;Inaugural lecture EUROMEDECINE 92, Montpellier, 1992 ; Special lecturededicated to the memory of Prof. Shosaku Numa, New York Academy of Sciences,Waseda University, Tokyo (Japan), 1993 ; Special lecture 11th European Workshopon Cognitive Neuropsychology, Accademia Cusano, Bressanone (Italy), 1993 ;Giuseppe Moruzzi lectures, Accademia Nazionale dei Lincei, Scuola NormaleSuperiore of Pisa, Italy, 1993 ; First Jus lecture on Ethics and Neurosciences,Toronto, 1995 ; Berlin Lecture in Molecular Medicine, Berlin (RFA), 1995 ; Sterlingdrug Lecture, Boston University School of medicine (USA), 1996 ; Flynn Lecture,Yale University, 1996 ; Cass Memorial Lecture, Dundee University, Scotland, 1996 ;Bruno Ceccarelli Lecture, Milan (Italy), 1996 ; First Cavalieri-Ottolenghi Lecture,Turin (Italy), 1996 ; EMBO Lecture : British Brain Research Association meeting,Liverpool (UK), 1997 ; Seventh annual Edmond Fischer Lecture, Seattle (USA),1997 ; Ralph I. Dorfman Memorial Lecture, Stanford Univ. School of Medicine(USA), 1998; Ferrier Lecture, The Royal Society, London (UK), 1998 ; EmanuelMerck-Vorlesung, Technische Universität, Darmstadt (RFA), 1998; Linus Paulinglecture, Stanford (USA), 1998/1999 ; F.C. Donders Lectures on cognitiveneuroscience, Nijmegen (NL), 1999 ; Burroughs-Wellcome lecture in Pharmacology,Washington, (USA), 1999 ; First Mind Brain and Behavior lectures, HarvardUniversity, (USA), 1999 ; Carl Friedrich Von Siemens Foundation lecture, Munich(RFA), 1999 ; Friday evening lecture, Woods Hole (USA), 2000 ; Annual Sterlinglecture, Albany Medical College, New York, 2001 ; Schueler distinguished lecture inpharmacology, New Orleans, (USA), 2002 ; Wenner-Gren distinguished lecture,Stockholm (Sweden), 2002 ; The Kenneth Myer Lecture, Melbourne (Australia),2003 ; The Heller Lecture Series in Computational Neuroscience, Institute of LifeSciences, Jerusalem (Israel), 2004 ; Jerry A. Weisbach memorial lecture, RockefellerUniversity, 2005 ; Benjamin W. Zwelfach Memorial Lecture, University ofCalifornia San Diego (USA), 2007 ; ASPET’s Centennial meeting, San Diego (USA)2008 ; Nobel symposium « Genes, Brain and Behavior », Stockholm, (Sweden) 2008 ;Keynote lecture CARTA Symposium « Evolutionary origins of Art and Aesthetics »,San Diego, (USA) 2009 ; Keynote lecture Keystone Symposium « Protein, dynamics,allostery and function », Keystone (USA) 2009 ; Inaugural Elaine Sanders-Bushlecture Vanderbilt University (USA) 2010 ; Open lecture Swedish Royal Academy ofSciences, Stockholm (Sweden) 2010 ; Nobel symposium « The Enlightened Brain»,Stockholm, (Sweden) 2010 ; Edwin G. Krebs Lecture on Molecular Pharmacology,Seattle (USA) 2011.6) Distinguished honorsGrand Croix dans l’Ordre National de la Légion d'Honneur, 2011; Grand-Croix dansl'Ordre National du Mérite 1995 ; Commandeur dans l'Ordre des Arts et des Lettres,1994 ; Commandeur des Palmes Académiques.7) Scientific societiesHonorary member of Neurosciences Research Program, MIT and RockefellerUniversity (USA), since 1984; Honorary member of the Japanese BiochemicalSociety, Sendai, Japan, 1985 ; Honorary member of the American NeurologyAssociation, 1988 ; Honorary member of University College London, 1990 ; Membred'honneur à titre étranger de la Société Belge de Neurologie, Bruxelles, 1991 ;Member of European Molecular Biology Organization.8) Administrative and scientific responsibilitiesMembre du Conseil Scientifique de l'Action Concertée Membranes Biologiques de laDélégation générale à la Recherche Scientifique et Technique (DGRST), 1969-1977 ;Membre de la Commission 6 de l'Institut National de la Santé et de la RechercheMédicale (INSERM), 1974- 1979 ; Membre du Conseil d'Administration del'Association des Pharmacologistes, 1978-1983 ; Président de l'Action Concertée"Dynamique du Neurone" (DGRST), 1977-1983 ; Membre de la Commission 22 duCentre National de la Recherche Scientifique (CNRS), "Interactions Cellulaires",1980-1982 ; Membre du Comité Sectoriel Sciences de la Vie (CNRS), 1981-1982 ;Vice-Président du Conseil Scientifique de la Fondation Fyssen, 1979-2000 ;Président du Conseil Scientifique de l'INSERM, 1983-1987 ; Membre du ConseilSupérieur de la Recherche et de la Technologie, 1987-1989 ; Membre du ConseilScientifique de l'Institut Pasteur, 1989-1992 ; Président de la Société desNeurosciences, 1989-1992 ; Président de la Commission Interministérielle pour laConservation du Patrimoine Artistique National, since 1989 ; Président de l'ActionConcertée "Sciences de la Cognition" du Ministère de la Recherche Scientifique etTechnique et du Ministère de l'Education Nationale, 1988-1992 ; Membre duConseil Scientifique de "Human Frontiers Science Program", 1990-1992 ; Membredu Comité Scientifique "Life Sciences" de l'European Science Foundation (ESF),1990-1992 ; Membre du Conseil du Développement Européen de la Science et de laTechnologie (CODEST), 1991-1992 ; Président du Comité Consultatif Nationald'Ethique pour les Sciences de la Vie et de la Santé, 1992-1998 ; Membre du Comitéde l'Energie Atomique 1998-2003 ; Membre du Conseil d’Administration del’Institut Pasteur, 2000-2005 ; Directeur du Département de Neuroscience InstitutPasteur, 2002- 2006 ; Président du Comité de Vigilance Ethique de l’InstitutPasteur, since 2007 ; Membre du Conseil Scientifique de l’Agence Internationale desMusées, France Muséums, since 2007 ; Membre du Comité de programmation duMusée du Luxembourg since 2010 ; Président du Conseil d’Orientation de l’Institutdu Cerveau et de la Moëlle épinière, La Salpétrière, 2010.22 23

9) Training and teachingJean-Pierre Changeux mentored more than 85 students and postdoctoral fellows,many of whomare now distinguished leaders in the fields of biological sciences,neuroscience in particular : Stanislas Dehaene (Prof Collège de France), ThierryHeidmann (médaille argent CNRS), Jérome Giraudat (médaille argent CNRS),Jacques Mallet, Nicolas LeNovère, Pierre-Jean Corringer, Uwe Maskos... in France,Jim Patrick (Prof Baylor college), Jonathan Cohen (Prof Harvard U), Henry Lester(Prof CalTech), Richard Olsen (Prof UCLA), Christopher Henderson (Prof ColumbiaU), Marina Picciotto (Prof Yale U)… in the USA. Naguib Mechawar (Prof McGill U)in Canada Katsuhiko Mikoshiba (Prof Tokyo U & Riken I) ; Vivian Teichberg (ProfWeizman I); Heinrich Betz (Prof Francfurt U)...10) Books and publicationsJ.-P. CHANGEUXL'Homme neuronal, Fayard Paris (1983) ; Neuronal Man (Laurence Gareytranslator) 1985 Pantheon Books;J.-P. CHANGEUXMolécule et Mémoire, Bedou Gourdon (1988)J.-P. CHANGEUX (dir.)Fondements naturels de l’Ethique, Odile Jacob Paris (1993)J.-P. CHANGEUX (dir.)Une même éthique pour tous? Odile Jacob Paris (1997)J.-P. CHANGEUX, A. CONNESMatière à pensée, Odile Jacob Paris (1989, 2000, 2008) ; Conversations on Mind,Matter and Mathematics (M.B. De Bevoise 1995 Princeton University Press;J.-P. CHANGEUXRaison et Plaisir, Odile Jacob Paris (1994, 2002)J.-P. CHANGEUX, P. RICOEURCe qui nous fait penser: La Nature et la Règle, Odile Jacob Paris (1998, 2008) ;What makes us think ? a neuroscientist philosopher argue about ethics, humannature and the brain (M.B. De Bevoise translator) (2000) Princeton UniversityPress;J.-P. CHANGEUXL’homme de vérité, Odile Jacob Paris (2002, 2004, 2008) ; The Physiology of Truth :neuroscience & human knowledge De Bevoise translator) Harvard UniversityPress;J.-P. CHANGEUX (dir.) Gènes et Culture, Odile Jacob Paris (2003)J.-P. CHANGEUX (dir.) La Vérité dans les sciences, Odile Jacob (2003)J.-P. Changeux & S. Edelstein Nicotinic acetylcholine receptors : from molecularbiology to cognition (2005) Odile Jacob J.-P. CHANGEUX catalogue d’expositionLa lumière au siècle des Lumières et aujourd’hui, Odile Jacob Paris (2005)J.-P. CHANGEUX catalogue d’expositionLes passions de l’âme, Odile Jacob Paris (2006)J.-P. CHANGEUX (dir.)L’Homme artificiel, Odile Jacob Paris, Colloque annuel du Collège de France (2007)J.-P. CHANGEUXDu vrai, du beau, du bien, Odile Jacob Paris (2008)More than 600 publications in international journals24

Invited SpeakersWired for sex: the neurobiologyof drosophila courtship behaviourWired for sex: the neurobiology of drosophila courtshipbehaviourBarry DicksonResearch Institute of Molecular PathologyBarry DicksonResearch Institute of Molecular PathologyHow are innate behavioural repertoires pre-programmed into the nervous system? Andhow does trial-and-error learning allow each individual to fine tune this innate templatesto adapt to the conditions of the local environment? The courtship behaviour ofDrosophila melanogaster males offers a tractable genetic model system to address thesequestions. I will present our efforts to define the anatomy and function of neural circuitythat generates male courtship behaviour, with a specific focus on the sexual dimorphismssculpted into these circuits by the fruitless gene, and how these sex differences may leadto male-specific generation of the courtship song. I will also discuss elements of thesecircuits that mediate learning in the adult fly, so that his courtship activity ispreferentially directed at the most appropriate target – the receptive virgin female.BiosketchBarry Dickson studied at the Universities of Melbourne and Queensland, graduating witha B.Sc. in computer science and a B.Sc.Hons. in genetics. After a brief period at the SalkInstitute in San Diego, he then moved for his PhD studies to the University of Zurich,Switzerland, where he worked with Ernst Hafen on receptor tyrosine kinase signallingduring Drosophila eye development. His postdoctoral work on axon pathfinding wasperformed with Corey Goodman at the University of California, Berkeley. In 1996 he setup his own group in Zurich, and in 1998 moved to Vienna, Austria, as a group leader atthe Research Institute of Molecular Pathology (IMP), where he is now the ScientificDirector.Barry’s research group has made key contributions to understanding the molecular andcellular mechanisms of axon pathfinding, in particular in the choices axonal growth conesas they navigate the midline of the Drosophila central nervous system. Recently, theirresearch focus has shifted to investigating how dedicated neural circuits mediate complexbehaviours, and how genes direct the assembly and function of these circuits. As a modelsystem, his group focuses on the innate reproductive behaviours of Drosophila.Selected recent publications1. Demir, E. and Dickson, B.J. (2005). fruitless splicing specifies male courtship behavior inDrosophila. Cell 121: 785-7942. Stockinger, P., Kvitsiani, D., Rotkopf, S., Tirian, L. and Dickson, B.J. (2005). Neuralcircuitry that governs Drosophila male courtship behavior. Cell 121: 795-8073. Kurtovic, A., Widmer, A., and Dickson, B.J. (2007). A single class of olfactory neuronsmediates behavioural responses to a Drosophila sex pheromone. Nature,446: 542-546.4. Dietzl, G., Chen, D., Schnorrer, F., Su, K.-C., Barinova, Y., Fellner, M., Gasser, B., Kinsey,K., Oppel, S., Scheiblauer, S., Couto, A., Marra, V., Keleman, K., and Dickson, B.J. (2007).A genome-wide transgenic RNAi library for conditional gene inactivation in Drosophila.Nature 448: 151-156.5. Keleman, K., Krüttner, S., Alenius, M., and Dickson, B.J. (2007). Function of theDrosophila CPEB protein Orb2 in long-term courtship memory. Nature Neuroscience 10:1587-1593..6. Yapici, N., Kim, Y.-J., Ribeiro, C., and Dickson, B.J. (2008). A receptor that mediates thepost-mating switch in Drosophila reproductive behaviour. Nature 451: 33-37.7. Häsemeyer, M., Yapici, N., Heberlein, U., and Dickson, B.J. (2009). Sensory neurons inthe Drosophila genital tract regulate female reproductive behavior. Neuron 61: 511-5188. Spitzweck, B., Brankatschk, M., Dickson, B.J. (2010). Distinct protein domains andexpression patterns confer divergent axon guidance functions for Drosophila Roboreceptors. Cell 140: 409-420.9. Yu, Y.J., Kanai, M.I., Demir, E., Jefferis, G.S.X.E., and Dickson, B.J. (2010). Cellularorganization of the neural circuit that drives Drosophila courtship behavior. Curr Biol. 20:1602-1614.10. von Philipsborn, A.C., Liu, T., Yu, J. Y., Masser, C., Bidaye, S.S. and Dickson, B.J. (2011).Neuronal control of Drosophila courtship song. Neuron 69: 509-522.2627

Invited SpeakersSignaling networks that regulatesynapse development and cognitive functionSignaling networks that regulate synapse developmentand cognitive functionMichael E. GreenbergHarvard Medical SchoolMichael E. GreenbergHarvard Medical SchoolOur interactions with the outside world trigger changes at neuronal synapses that arecritical for proper brain development and higher cognitive function. Research in theGreenberg laboratory has focused on the identification of a genetic program that isactivated by neuronal activity, the mechanisms of signal transduction that carry theneuronal activity-dependent signal from the membrane to the nucleus, and theidentification of regulators of this experience-dependent process that affect synapsedevelopment and plasticity. Our recent studies using global screening techniques haveidentified a number of activity-dependent genes that control various processes such as1) the complexity of the dendritic arbor, 2) the formation, maturation, and maintenanceof spines, the post-synaptic sites of excitatory synapses, 3) the composition of proteincomplexes at the pre- and post-synaptic sites, 4) the relative number of excitatory andinhibitory synapses, and 5) the production and secretion of neuropeptides that controlsynaptic inhibition. These activity-regulated processes are critical for normal braindevelopment and function, and defects in the activity-dependent gene programcontribute to disorders of human cognition such as Rett Syndrome (RTT) and AngelmanSyndrome (AS), two neurological disorders associated with syndromic autism.Understanding how the neuronal activity-dependent gene program functions mayprovide insight into how the dysregulation of this process leads to neurological diseasesand, ultimately, may suggest therapies for treatment of disorders of cognitive function.Michael E. Greenberg, Ph.D.Nathan Marsh Pusey Professor of NeurobiologyChair, Department of NeurobiologyHarvard Medical SchoolMichael E. Greenberg, PhD was named Chair of the Department of Neurobiology andNathan Marsh Pusey Professor in September, 2008. He came to Harvard Medical Schoolfrom Children’s Hospital Boston, where he directed the F.M. Kirby Neurobiology Center.Dr. Greenberg’s selection as chair reflects his unique qualification to lead the department ata pivotal moment in the field of neuroscience, when understanding of the nervous system ata molecular, cellular and physiological level is increasingly translating to direct influenceon the treatment of neurologic and psychiatric disease.Dr. Greenberg’s own research has expanded understanding of the molecular basis of themajor events in neural development, the neural responses to injury and disease, and thepotential for intervention, treatment, or cure. His research has also explored the molecularbiology and genetics of autism spectrum disorders. More specifically, Dr. Greenberg and hisresearch group focus on identifying mechanisms that trigger proliferation, differentiationand survival of neurons during development, and adaptive responses in the mature nervoussystem. Their work has uncovered the existence and function of a genetic program that isactivated by neuronal activity, the mechanisms of signal transduction that carry the neuronalactivity-dependent signal from the membrane to the nucleus, and the identification ofregulators of this experience-dependent process that affect synapse development andplasticity. Professor Greenberg is particularly interested in those activity-dependentprocesses whose dysfunction can lead to the development of diseases of cognitive function.Dr. Greenberg currently serves on the editorial boards of Neuron, Journal of Neuroscience,Learning & Memory, and Molecular & Cellular Neuroscience. He is the recipient ofnumerous honors and awards, including membership in both the American Academy of Artsand Sciences and the National Academy of Science. He is also the recipient of theMcKnight Innovation in Neuroscience Award, the Edward M. Scolnick Prize inNeuroscience, and the A. Clifford Barger Award for Excellence in Mentoring, a prize givenannually by Harvard Medical School to faculty members who have established a long-termcommitment to fostering strong mentoring relationships with students, trainees, and juniorfaculty.Professor Greenberg graduated Magna Cum Laude from Wesleyan University, and receivedhis Ph.D. from Rockefeller University.2829

Program Director/Principal Investigator (Last, First, Middle):BIOGRAPHICAL SKETCHProvide the following information for the Senior/key personnel and other significant contributors in the order listed on Form Page 2.Follow this format for each person. DO NOT EXCEED FOUR PAGES.NAMEMichael E. GreenbergeRA COMMONS USER NAME (credential, e.g., agency login)MiGreenbergPOSITION TITLEProfessor of NeurobiologyHead of the Department of Neurobiology, HarvardMedical SchoolEDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, include postdoctoral training andresidency training if applicable.)INSTITUTION AND LOCATIONDEGREE(if applicable)MM/YYFIELD OF STUDYWesleyan University, Middletown, CT B.A. 05/76 ChemistryThe Rockefeller University, New York, NY Ph.D. 06/82 BiochemistryA. Personal StatementOver the last two decades Dr. Greenberg has served as a leader in the field of molecular neurobiology. Hisresearch has revealed a complex activity-regulated gene expression program relevant to synapsedevelopment and neural circuitry. His research contributes greatly to our understanding of diseases ofcognition in which these processes of synapse development and neural circuit formation have gone awry.B. Positions and Honors.Positions and Employment1983-1986 Postdoctoral Fellow with Dr. Edward B. Ziff, Department of Biochemistry, New York UniversityMedical Center (New York, NY)1986-1991 Assistant Professor, Department of Microbiology and Molecular Genetics, Harvard MedicalSchool (Boston, MA)1991-1993 Associate Professor, Department of Microbiology and Molecular Genetics, Harvard MedicalSchool (Boston, MA)1993-1994 Professor, Department of Microbiology and Molecular Genetics, Harvard Medical School(Boston, MA)1994-2008 Professor, Department of Neurology and Neurobiology, Harvard Medical School and Director,Neurobiology Program, Children's Hospital (Boston, MA)2008- Nathan Marsh Pusey Professor of Neurobiology, Chair of the Department of Neurobiology,Harvard Medical School (Boston, MA)Other Experience and Professional Memberships1990- Editorial Boards: Neuron; J. Neuroscience, Learning & Memory; Mol. & Cell Neuroscience;Molecular & Cellular Biology1992-1996 Member/Chair, National Institutes of Health Neurology C Study Section1993-2006 Member/Chair, Medical Foundation/Charles A. King Trust Study Section1996-2006 Scientific Advisory Board, Upstate Biotechnology Inc.1991-2001 Scientific Advisory Board, Helicon Inc.1998-2002 Scientific Advisory Board, Cogent Neuroscience, Inc.2008- Scientific Advisory Board, Constellation2008- International Science Advisory Council2008- Harvard University Science and Engineering Committee (HUSEC)Honors1976 Phi Beta Kappa, Sigma Xi, B.A. Magna Cum Laude, Honors in Chemistry1983-1984 Damon Runyon-Walter Winchell Postdoctoral Fellowship1987-1990 Searle Scholars Program Award--Chicago Community TrustProgram Director/Principal Investigator (Last, First, Middle):1990-1993 McKnight Scholars Award in Neuroscience2006 A. Clifford Barger Award for Excellence in Mentoring—Harvard Medical School2006 3 rd Annual Edward M. Scolnick Prize in Neuroscience (McGovern Institute)2007 Harvey Lecture (Rockefeller University)2008 J. Allyn Taylor International Prize in Medicine2008 Elected to the National Academy of Sciences2009 Perl-UNC Neuroscience Prize2009 Julius Axelrod Prize2010 Vernon B. Mountcastle Lecture (Johns Hopkins University)2010 Walter Massey Family Lecture (Marine Biological Laboratory, Woods Hole, MA)C. Selected peer-reviewed publications (selected from >170 total)1. Dolmetsch RE, Urvi P, Fife K, Spotts JM, Greenberg ME. Signaling to the nucleus by an L-type calciumchannel-calmodulin complex through the MAP Kinase Pathway (Research Article). Science 2001; 294:333-339.2. Tran H, Brunet A, Grenier JM, Data SR, Fornace AJ Jr, DeStefano PS, Chiang LW, Greenberg ME. DNArepair pathway stimulated by the forkhead transcription factor FOXO3a (FKHRL1) through the Gadd45protein. Science 2002; 296(5567): 530-540.3. Kornhauser JM, Cowan CW, Shaywitz AJ, Dolmetsch RE, Griffith EC, Hu LS, Haddad C, Xia Z, GreenbergME. CREB transcriptional activity in neurons is regulated by multiple, calcium-specific phosphorylationevents. Neuron 2002; 34(2): 221-233.4. Datta SR, Ranger AM, Lin MZ, Sturgill JF, Ma YC, Cowan CW, Dikkes P, Korsmeyer SJ, Greenberg ME.Survival factor-mediated BAD phosphorylation raises the mitochondrial threshold for apoptosis.Developmental Cell 2002; 3(5): 631-643.5. Chen WG, Chang Q, Lin Y, Meissner A, West AE, Griffith EC, Jaenisch R, Greenberg ME. Derepressionof BDNF transcription involves calcium-dependent phosphorylation of MeCP2. Science 2003; 302(5646):885-889.6. Brunet A, Sweeney LB, Sturgill JF, Chua KF, Greer PL, Lin Y, Tran H, Ross SE, Mostoslavsky R, CohenHY, Hu LS, Cheng HL, Jedrychowski MP, Gygi SP, Sinclair DA, Alt FW, Greenberg ME. Stress-dependentregulation of FOXO transcription factors by the SIRT1 deacetylase. Science 2004; 303(5666): 2011-2015.7. Tolias KF, Bikoff JB, Burette A, Paradis S, Harrar D, Tavazoie S, Weinberg RJ, Greenberg ME. The Rac1-GEF Tiam1 couples the NMDA receptor to the activity-dependent development of dendritic arbors andspines. Neuron 2005; 45(4): 525-538.8. Cowan CW, Shao YR, Sahin M, Shamah SM, Lin MZ, Greer PL, Gao S, Griffith EC, Brugge JS,Greenberg ME. Vav family GEFs link activated Ephs to endocytosis and axon guidance. Neuron 2005;46(2): 205-2179. Schratt GM, Tuebing F, Nigh EA, Kane C, Sabatini ME, Kiebler M, Greenberg ME. A brain-specificmicroRNA regulates dendritic spine development. (Article) Nature 2006; 439(7074): 283-289.10. Ma YC, Song MR, Park JP, Henry Ho HY, Hu L, Kurtev MV, Zieg J, Ma Q, Pfaff SL, Greenberg ME.Regulation of motor neuron specification by phosphorylation of neurogenin 2. Neuron. 2008; 58(1): 65-77.11. Lin Y, Bloodgood, BL, Hauser JL, Lapan, AD, Koon, AC, Kim T-K, Hu LS, Malik AN, Greenberg ME.Activity-dependent regulation of inhibitory synapse development by Npas4. (Article) Nature, 2008;455(7217): Program 1198-1204. Director/Principal PMCID: Investigator PMC2637532(Last, First, Middle):12. Flavell SW, Kim TK, Gray JM, Harmin DA, Hemberg M, Hong EJ, Markenscoff-Papadimitriou E, Bear DM,PHS 398/2590 (Rev. 06/09) Page Continuation Format PageGreenberg ME. Genome-wide analysis of MEF2 transcriptional program reveals synaptic target genes andneuronal activity-dependent polyadenylation site selection. Neuron 2008; 60(6): 1022-1038. PMCID:PMC263017813. Greer PL, Hanayama R, Bloodgood BL, Mardinly AR, Lipton DM, Flavell SW, Kim TK, Griffith EC, WaldonZ, Maehr R, Ploegh HL, Chowdhury S, Worley PF, Steen J, Greenberg ME. The Angelman Syndromeprotein Ube3A regulates synapse development by ubiquitinating Arc. Cell 2010; 140(5): 704-716. PMCID:PMC284314314. Ross SE, Mardinly AR, McCord AE, Zurawski J, Cohen S, Jung C, Hu L, Mok SI, Shah A, Savner EM,Tolias C, Corfas R, Chen S, Inquimbert P, Xu Y, McInnes RR, Rice FL, Corfas G, Ma Q, Woolf CJ,Greenberg ME. Loss of inhibitory interneurons in the dorsal spinal cord and elevated itch in Bhlhb5 mutantmice. Neuron 2010; 65(6): 886-898. PMCID: PMC2856621PHS 1991-1996 398/2590 (Rev. American 06/09) Cancer Society Faculty Research Page Award1999-2001 McKnight Innovation in Neuroscience AwardBiographical Sketch Format Page1999-2006 Jacob Javits Neuroscience Award2001-2003 Ellison Medical Foundation Senior Scholar’s Award2003 Election to the American Academy of Arts and Sciences2006 A. Clifford Barger Award for Excellence in Mentoring—Harvard Medical School2006 3 rd Annual Edward M. Scolnick Prize in Neuroscience (McGovern Institute)2007 Harvey Lecture (Rockefeller University)2008 J. Allyn Taylor International Prize in Medicine2008 Elected to the National Academy of Sciences2009 Perl-UNC Neuroscience Prize2009 Julius Axelrod Prize2010 Vernon B. Mountcastle Lecture (Johns Hopkins 30 University)2010 Walter Massey Family Lecture (Marine Biological Laboratory, Woods Hole, MA)3115. Kim TK, Hemberg M, Gray JM, Costa AM, Bear DM, Wu J, Harmin DA, Laptewicz M, Barbara-Haley K,Kuersten S, Markenscoff-Papadimitriou E, Kuhl D, Bito H, Worley PF, Kreiman G, Greenberg ME.Widespread transcription at neuronal activity-regulated enhancers. (Article) Nature 2010; 465(7295): 182-187. NIHMSS 233355

Invited SpeakersKinesin superfamily molecular motors (KIFs)as key regulators for intracellular transportand function higher brain functionKinesin superfamily molecular motors (KIFs) as keyregulators for intracellular transport and higher brainNobutaka HirokawaDepartment of Cell Biology and Anatomy, Graduate School of Medicine,University of TokyoNobutaka HirokawaDepartment of Cell Biology and Anatomy, Graduate School of Medicine, University of TokyoAbstract: Kinesin superfamily motor proteins, KIFs play fundamental roles on theneuronal functions and survival by transporting various cargos, such as synapticvesicle precursor, mitochondria, plasma membrane protein vesicles, proteincomplexes, vesicles containing receptors, and mRNAs with large protein complex inthe axon and dendrites. KIF 1A and KIF1B beta transport synaptic vesicleprecursors in the axon and KIF 17 transports vesicles containing NMDA typeglutamate receptors in dendrites. In this symposium first I will focus on themechanisms how KIF1A/1B beta and KIF 17 recognize the cargoes and unload them.KIF1A/1B beta bind DENN/MADD through their stalk region and DENN/MADDrecognizes and binds Rab3 in the synaptic vesicle precursor. The binding to Rab3is controlled by GTP-hydrolysis. GTP-Rab3 can bind DENN/MADD, whileGDP-Rab3 cannot. In the case of KIF 17 KIF 17 binds Mint-1(mLin10) andrecognizes and binds NR2B in the cargo vesicle through interaction with scaffoldprotein complex containing Mint-1. The interaction between KIF 17 and Mint- 1 iscontrolled by phosphorylation of KIF17 tail by CaMKIIalpha. CaMKIIalpha bindsKIF17 tail domain and phosphorylates S1029. Then Mint-1 is released from KIF 17.Thus the mechanisms coupled with hydrolysis of small G-protein in the cargos andphosphorylation of KIF have been identified as the mechanisms to unload cargos.Second, I will introduce in vivo function of KIF 17. Disruption of kif17 gene inhibitsNR2B transport, accompanied by decreased transcription of nr2b, resulting in a lossof synaptic NR2B. In kif17-/- hippocampal neurons, the NR2A level is alsodecreased because of accelerated ubiquitin proteasome system-dependentdegradation. Accordingly, NMDA receptor-mediated synaptic currents, early andlate long-term potentiation, long-term depression, and CREB responses areattenuated in kif17-/- neurons, concomitant with a hippocampus-dependent memoryimpairment in knockout mice. In wild-type neurons, CREB is activated by synapticinputs, which increase the levels of KIF17 and NR2B. Thus, KIF17 differentiallymaintains the levels of NR2A and NR2B, and, when synapses are stimulated, theNR2B/KIF17 complex is upregulated on demand through CREB activity. TheseKIF17-based mechanisms for maintaining NR2A/2B levels could underlie multiplephases of memory processes in vivo. Further, as the last subject I will introducesignificant unexpected functions of KIFs revealed by molecular genetics. KIF2A isfundamental for neuronal migration and brain wiring by depolymerizingmicrotubules in growth cones and suppressing unnecessary elongation of axoncollaterals. KIF4 controls the activity-dependent survival of neurons by regulatingPARP-1 activity during brain development. KIF26A controls development of entericnervous system as a key suppressor of GDNF/Ret signaling cascade. Thus, KIFsplay a number of significant roles not only on various neuronal functions bytransporting important cargos, but also on fundamental physiological processessuch as higher brain function, brain wiring, and CNS/PNS development.Biography: Nobutaka Hirokawa graduated from the School of Medicine at theUniversity of Tokyo in 1971. He received Ph D degree from the University's Facultyof Medicine in 1978. He did postdoctoral work at the University of California at SanFrancisco and Washington University School of Medicine in St. Louise and becamea Research Assistant Professor of Physiology and Biophysics there (1981-83), andthen an Associate Professor of Anatomy and Neurobiology (1983). From 1983 until2009 he has served at the Graduate School of Medicine at the University of Tokyo asa Professor and Chairman of the Department of Cell Biology and Anatomy. From2003 April to 2007 March he was also appointed as the dean of Graduate School ofMedicine, University of Tokyo. He is now a project professor in University of Tokyo,Graduate School of Medicine. He is a member of Japan Academy and an electedassociate member of EMBO. Widely respected in international circles, Hirokawahas been on the editorial boards of many international top journals including Cell,Science, Neuron, Dev Cell, J Cell Biol, EMBO J, Curr Opi Cell Biol, and Trends inCell Biol. (http://cb.m.u-tokyo.ac.jp)Recent Publication:1. Tanaka, Y., Y. Okada, and N. Hirokawa. Nature, 435: 172-177, 2005.2. Okada, Y., S. Takeda, Y. Tanaka and N. Hirokawa. Cell, 121 : 633-644, 20053. Hirokawa, N., Y. Tanaka, Y. Okada and S. Takeda. Cell 125 (1): 33-45, 2006.4. Midorikawa R., Y. Takei, and N. Hirokawa. Cell 125: 371-383, 2006.5. Guilaud, L., R. Wong and N. Hirokawa. Nature Cell Biol 10 (1): 19-29, 2008.6. Niwa, S., Y. Tanaka and N. Hirokawa. Nature Cell Biol 11: 1270-1276, 2008.7. Hirokawa, N., Y. Noda, Y. Tanaka, and S. Niwa. Nature Rev Mol Cell Biol. 10: 682-696,2009.8. Zhou R., S. Niwa, N. Homma, Y. Takei, and N. Hirokawa. Cell 139 (4): 802-813, 2009.9. Hirokawa, N., S. Niwa and Y. Tanaka. Neuron 18; 610-638, 2010.10. Yin, X,. Y. Takei, M. Kido and N. Hirokawa. Neuron 70: 310-325, 20113233

Invited SpeakersSynaptic competition in the dendritic spinesof CA1 pyramidal neuronsSynaptic competition in the dendritic spines of CA1pyramidal neuronsHaruo KasaiDepartment of Structural Physiology, Graduate School of Medicine,The University of TokyoHaruo KasaiDepartment of Structural Physiology, Graduate School of Medicine, The University of TokyoCompetitive stabilization and elimination of synaptic connections play key role in therefinement of neuronal networks during development, learning andmemory_ENREF_2. Biological processes underlying the synaptic competition,however, have been poorly understood. In the cerebral cortex, excitatory synapses areformed on small protrusions of dendrites, dendritic spines, in the pyramidal neurons.Selection of dendritic spines is achieved by structural plasticity of dendritic spines,their enlargement, shrinkage, which are associated with long-term potentiation (LTP)and depression (LTD), respectively_ENREF_4. Two-photon uncaging of glutamaterevealed that long-lasting plasticity of excitatory synapses, i.e. long-term potentiation,can be induced at the level of single spines and is associated with spine enlargement(1,4-9). In contrast, although spine shrinkage can be induced with electrical stimulationof presynaptic fibers, no one has succeeded in induction of spine shrinkage bystimulation of identified spines, which has hampered understanding of synapticcompetition. Here we report that spine shrinkage could be robustly induced whenGABA inhibition (2) was applied to a dendrite during the spike-timing protocol forinduction of LTD. Such spine shrinkage spread to the neighboring spines readily over10 μm, and competed with the spine enlargement. In contrast, the spine enlargementnever spread to the neighboring spines, and did neither induce nor suppress shrinkageof surrounding spines. Thus, the spine synapses tightly interacted each other forcompetitive selection of synapses owing to the spread of spine shrinkage, whileindividual modifiability of synapse was preserved because spine enlargement isconfined. Such spine shrinkage was dependent on GABA A receptors, which likelysuppress dendritic Ca 2+ influx following action potential. We will introduce themolecular mechanisms underlying both the spread of shrinkage and the confinement ofenlargement of dendritic spines in CA1 pyramidal neurons.1981 Graduated from the University of Tokyo, Faculty of Medicine.1988-1990 Humboldt Fellow in the Max-Planck Institute.1993-1999 Associate Professor in the University of Tokyo.1999-2005 Professor, National Institute for Physiological Sciences.2005-Present Professor in the University of TokyoReferences:1. Noguchi, J., Nagaoka, A., Watanabe, S., Ellis-Davies, G.C.R., Kitamura, K., Kano,M., Matsuzaki, M. & Kasai H. In vivo two-photon uncaging of glutamate revealingthe structure-function relationships of dendritic spines in the neocortex of adultmice. J.Physiol. 589: 2320-2329, 2011.2. Kanemoto, Y., Matsuzaki, M., Morita, S., Hayama, T., Noguchi, J., Senda, N.,Momotake, A., Arai, T., and Kasai, H. Spatial distributions of GABA receptors andlocal inhibition of Ca 2+ transients studied with GABA uncaging in the dendrites ofCA1 pyramidal neurons. PLoS ONE, 6: e22652, 2011.3. Matsuzaki, M., Ellis-Davies, G.C.R., Kanemoto, Y., & Kasai, H. Simultaneoustwo-photon activation of presynaptic cells and calcium imaging in postsynapticdendritic spines. Neural Systems and Circuits 1:2, 2011.4. Kasai, H., Hayama, T., Ishikawa, M., Watanabe, S. & Yagishita, S. Learning rules andpersistence of dendritic spines. Eur. J. Neurosci. 32, 241-249, 2010.5. Kasai H, Fukuda M, Watanabe S, Hayashi-Takagi A & Noguchi J: Structuraldynamics of dendritic spines in memory and cognition. Trends Neurosci 33:121-129, 2010.6. Tanaka J, Horiike Y, Matsuzaki M, Miyazaki T, Ellis-Davies GCR & Kasai HProtein synthesis and neurotrophin-dependent structural plasticity of singledendritic spines. Science 319:1683-1687, 2008.7. Honkura, N., Matsuzaki, M., Noguchi, J., Ellis-Davies,G.C.R. & Kasai, H. Thesubspine organization of actin fibers regulates the structure and plasticity ofdendritic spines. Neuron 57, 719-729, 2008.8. Noguchi, J., Matsuzaki, M., Ellis-Davies, G.C.R. & Kasai, H. (2005). Spine-neckgeometry determines NMDA receptor–dependent Ca 2+ signaling in dendrites.Neuron 46, 609-622.9. Matsuzaki M, Honkura N, Ellis-Davies GCR & Kasai H Structural basis of long-termpotentiation in single dendritic spines. Nature 429: 761-766, 2004.3435

Invited SpeakersEvolution of olfactory receptor gene repertoiresand functionEvolution of olfactory receptor gene repertoires and functionSigrun KorschingInstitute of Genetics, University at Cologne, Cologne, GermanySigrun KorschingInstitute of Genetics, University at Cologne, Cologne, GermanyMost olfactory receptor gene families evolve rapidly, following a birth-and-death mode of evolution.It is widely assumed that the purpose of such dynamic evolution is adaptation to species-specificecological niches and communication signals. We have phylogenetically characterized the fish taargene family and find this family to be an extreme example of evolutionary dynamics, with severalinstances of positive selection. At the other extreme lies the V1R-related ora gene family, which wefound to be highly conserved, with orthologues of individual genes detectable in species as far apartas shark, zebrafish and frog. We have begun to deorphanize receptors from both families.Preliminary observations are consistent with the hypothesis that the evolutionary dynamic ofreceptor genes does not correspond to a similar dynamic in biological function.Name:Address:Dr. Sigrun KORSCHINGInstitut für Genetik, Universität zu Köln, D-50674 Köln, DeutschlandDr. Korsching obtained her Ph.D. (summa cum laude) 1984 from the Ludwigs-Maximilians-Universität Munich in the research field of neurotrophic factors, with Prof. Hans Thoenen asscientific advisor. For this work she received the Otto-Hahn-Medal of the Max-Planck-Society. Sheextended her studies in this field during a postdoc period at the California Institute of Technology,USA. While a junior group leader at the Max-Planck-Institut für Entwicklungsbiologie, Tübingen,Dr. Korsching began to investigate the sense of smell. 1995 she became professor at the Institute ofGenetics, University of Cologne, and 1996 she habilitated in "Biochemistry and Molecular Biology"at the Faculty of Chemistry and Pharmacy, University of Tübingen. She has been board member ofthe German Neuroscience Society (NWG) for several years and has served as President of thissociety 2009-2011.Dr. Korschings current research interests center on the question of how odors are recognized,represented and perceived within the nervous system, and in particular on the evolution of thesemechanisms in vertebrates. She has made several contributions to the field of olfactory coding,demonstrating individually identifiable glomeruli in the vertebrate olfactory bulb (1), showingfuzzy spatial segregation in teleost odorant receptor expression domains (2), and showing bothcombinatorial and labeled line coding in vertebrates (3, 4). In depth studies of the molecularproperties guiding odor representation in the olfactory bulb followed (5, 6). Recently, shediscovered an unexpectedly conserved fish olfactory receptor gene family (7), which despite itssmall size of just 6 genes comprises the large family of mammalian V1R receptors as a singlesubclade. Further phylogenetic studies have led to a reappraisal of the origin and evolutionarydynamics of another olfactory receptor family (8) and to the discovery of a whole new class ofG{alpha} proteins (9). Recently she reported a novel type of olfactory receptor gene expression, a'one cell type – one receptor' mode of expression (10).10. Oka Y., Saraiva L.R., Korsching S.I. Crypt neurons express a single V1R-related ora gene,Chem. Senses advance access 29.10. 2011.9. Oka, Y., Saraiva, L. R., Kwan, Y. Y. & Korsching, S. I. (2009) The fifth class of G{alpha}proteins. Proc Natl Acad Sci U S A 106, 1484-9.8. Hussain, A., Saraiva, L. & Korsching, S. I. (2009) Positive selection and the birth of anolfactory receptor clade in teleosts. Proc Natl Acad Sci USA 106, 4313–4318.7. Saraiva, L. R. & Korsching, S. I. (2007) A novel olfactory receptor gene family in teleost fish.Genome Res 17, 1448-57.6. Fuss, S. H. & Korsching, S. I. (2001) Odorant feature detection: activity mapping of structureresponse relationships in the zebrafish olfactory bulb. J Neurosci 21, 8396-407.5. Fried, H. U., Fuss, S. H. & Korsching, S. I. (2002) Selective imaging of presynaptic activity inthe mouse olfactory bulb shows concentration and structure dependence of odor responses inidentified glomeruli. Proc Natl Acad Sci U S A 99, 3222-7.4. Friedrich, R. W. & Korsching, S. I. (1998) Chemotopic, Combinatorial, and NoncombinatorialOdorant Representations in the Olfactory Bulb Revealed Using a Voltage-Sensitive AxonTracer. J Neurosci. 18, 9977-88.3. Friedrich, R. W. & Korsching, S. I. (1997) Combinatorial and Chemotopic Odorant Coding Inthe Zebrafish Olfactory Bulb Visualized By Optical Imaging. Neuron 18, 737-752.2. Weth, F., Nadler, W. & Korsching, S. (1996) Nested expression domains for odorant receptorsin zebrafish olfactory epithelium. Proc Natl Acad Sci U S A 93, 13321-6.1. Baier, H. & Korsching, S. (1994) Olfactory glomeruli in the zebrafish form an invariant patternand are identifiable across animals. J Neurosci 14, 219-230.3637

Invited SpeakersCalreticulin chaperones regulate functionalexpression of V2R pheromone receptorsCalreticulin chaperones regulate functional expression of V2Rpheromone receptorsHiroaki MatsunamiDuke University Medical CenterHiroaki MatsunamiDuke University Medical CenterAbstract:Intraspecific communication in animals is often mediated by pheromones, partly detected by theaccessory olfactory organ, the Vomeronasal Organ (VNO) in mammals. Previous studies haveuncovered molecules that are specifically expressed in the VNO, including three independent groups ofputative pheromone receptors, the V1Rs, the V2Rs and the Fprs.The V2Rs are thought to detect peptide cues from other animals. However, no specific ligand-receptorpairs have been demonstrated heterologously, partly because V2Rs are difficult to study since they failto traffic to the surface of heterologous cells.The VNO appears to be vestigialized in humans and the vast majority of the V1Rs and all of theV2Rs as well as the VNO-specific ion channel, Trpc2, are pseudogenes in the human genome. Wehypothesized that genes that have specific functions in the VNO are pseudogenized in humans. Weused a published list of human pseudogenes to identify intact orthologues in mouse and asked if any ofthem might be specifically expressed in the VNO. We performed RT-PCR and in situ hybridization toassay transcription of these genes in different mouse tissues and found calreticulin 4, a homologue ofcalreticulin, with highly enriched expression in the mouse VNO. In contrast, the ubiquitously expressedcalreticulin expression is diminished in the VNO.Reducing calreticulin expression causes the unfolded protein response that is suppressed bycalreticulin4 in HEK293T cells. Depleting calreticulin expression in HEK293T cells enhances thetrafficking of V2Rs to the cell surface, while overexpression of calreticulin4 has no effects. Using thisknowledge, we have established a system to monitor the ligand interaction with V2Rs and demonstratethat ESP family members can activate V2Rs. Our results provide a platform to characterize the cognateligands of V2Rs in the heterologous system.NAMEHiroaki MatsunamiBIOGRAPHICAL SKETCHPOSITION TITLEAssociate Professor of Molecular Genetics andMicrobiologyAssociate Professor of NeurobiologyEDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, and include postdoctoral training.)INSTITUTION AND LOCATIONDEGREE(if applicable)YEAR(s)FIELD OF STUDYKyoto University, Kyoto, Japan BS 1991 BiologyKyoto University, Kyoto, Japan MS 1993 BiophysicsKyoto University, Kyoto, Japan PhD 1996 BiophysicsHarvard Medical School Postdoctoral 2001 NeurobiologyPositions and Employment1990-1991 Undergraduate Student, Department of Biophysics, Faculty of Science, Kyoto University1991-1996 Graduate Degree Researcher, Dept. of Biophysics, Faculty of Science, Kyoto University1996-2000 Postdoctoral fellow, Department of Neurobiology, Harvard Medical School2001-2008 Assistant Professor, Department of Molecular Genetics and Microbiology, Duke UniversityMedical Center2008-present Associate Professor (with Tenure), Department of Molecular Genetics and Microbiology, DukeUniversity Medical CenterRecent publications1. Dey, S. and Matsunami, H. Calreticulin chaperones regulate functional expression of vomeronasal type 2pheromone receptors. Proc Natl Acad Sci U S A 2011, 108, 16651-16656.2. Li, Y.R. and Matsunami, H. Activation state of the M3 muscarinic acetylcholine receptor modulatesmammalian odorant receptor signaling. Science Signaling, 2011, 4, ra13. Saito, H*., Chi, Q., Zhuang, H., Matsunami, H., and Mainland, J.* Odor Coding by a Mammalian ReceptorRepertoire. Science Signaling 2009, 2, ra94. Zhuang, H, Chien, M., and Matsunami, H. Dynamic Functional Evolution of an Odorant Receptor forSex-steroid Derived Odors in Primates. Proc Natl Acad Sci U S A 2009, 21247-515. Zhuang, H., and Matsunami, H. Evaluating cell-surface expression and measuring activation of mammalianodorant receptors in heterologous cells. Nature Protocols 2008 3, 1402-1413 (PMCID: PMC2664838)6. Keller, A.*, Zhuang, H.*, Chi, Q., Vosshall, L. B., and Matsunami, H. Genetic variation in a human odorantreceptor alters odour perception. Nature, 2007 449, 468-4727. Hu, J., Zhong, C., Ding C., Chi, C., Walz, A., Mombaerts, P., Matsunami, H., and Luo, M. Detection ofatmospheric concentrations of carbon dioxide by an olfactory subsystem in the mouse. Science 2007 317,953-9578. Zhuang, H., and Matsunami, H. Synergism of accessory factors in functional expression of mammalianodorant receptors. J Biol Chem. 2007 282, 15284-152939. Ishimaru, Y., Inada, H., Kubota, M., Zhuang, H., Tominaga, M., and Matsunami, H. Transient receptorpotential family members PKD1L3 and PKD2L1 form a candidate sour taste receptor. Proc Natl Acad Sci U SA 2006 103, 12569-12574.10. Saito, H., Kubota, M., Roberts, R. W., Chi, Q., and Matsunami, H: RTP family members induce functionalexpression of mammalian odorant receptors. Cell 2004 119, 679-691.*equal contribution3839

Invited SpeakersCognitive developmentin humans and chimpanzeesCognitive development in humans and chimpanzees Tetsuro MatsuzawaTetsuro MatsuzawaKyoto UniversityKyoto UniversityThe human mind is a product of evolution, much like the human body. Theevolutionary history of the body can be reconstructed from the fossil record – fromancient skulls, bones, and teeth. However, the mind does not fossilize. Therefore, toexplore the evolution of the human mind, comparative work is needed that uses thecognitive world of closely-related species – such as chimpanzees – as a reference point,or an “out-group” for comparison. I have been studying chimpanzees both in Japan andin Africa. The research project, known as the “Ai-project”, began in 1978. In parallel tothe laboratory work, I have visited Africa each year since 1986 to study wildchimpanzees in their natural habitat. Just like us, chimpanzees acquire many newskills as they mature. In this context, the key issue concerns the mechanisms behindthe accumulation of knowledge and technology independent of genetic channels. Whatis acquired? When? How? Fieldwork at Bossou provides an excellent setting in whichchimpanzees’ cognitive development can be observed across three generations. We haveindividual longitudinal records for 13 chimpanzees in a community that has beenmonitored continuously since 1976. The laboratory at the PRI, Kyoto University, can inturn provide complementary data on the development and detailed features ofchimpanzee cognition examined under strictly controlled conditions. In addition to thestudy of chimpanzees (Pan troglodytes), we have just started the new research onbonobos (Pan paniscus) both in the laboratory and in the wild. This represents thefirst ever attempt to compare chimpanzees and bonobos across the two differentresearch settings, and will provide us with a novel and comprehensive picture of thecommon ancestor of the genus Pan. Systematic comparisons of the three hominidspecies (humans, chimpanzees, and bonobos) will shed new light on the evolutionaryorigins of the human mind, technology, education, culture, mother-infant bond, andsociety.Name: Tetsuro MatsuzawaAffilliation: Primate Research Institute, Kyoto UniversityBrief Biography2006(Apr)-: Director, Primate Research Institute, Kyoto University.1993(Sep)-: Professor, Primate Research Institute, Kyoto University.1989(Mar): Ph.D. Science, Kyoto University.1987(Sep)-1993(Aug): Associate Professor, Primate Research Institute, Kyoto University.1985(Jun)-1987(Apr): Visiting Researcher, University of Pennsylvania, PA, USA1976(Dec)-1987(Aug): Assistant Professor, Primate Research Institute, Kyoto University.1974(Apr)-1976(Nov): Graduate School of Letters, Kyoto UniversityI have been studying captive chimpanzees from comparative cognitive perspectives.The “Ai project” continues since 1978. Other activities include observations of wildchimpanzees at Bossou and Nimba, Guinea, West Africa since 1986. The more recentfocus is wild orangutans in Borneo, wild bonobos in Congo, and wild gorillas in Rwanda.The key question is what is uniquely human. The answer is expected to come from thecomparison of humans and nonhuman primates.List of recent publications1. Matsuzawa, T., Humle, T. & Sugiyama, Y. (eds.) (2011). Chimpanzees of Bossou andNimba. Springer.2. Martin, C., Biro, D. & Matsuzawa T. (2011). Chimpanzees' use of conspecific cues inmatching-to-sample tasks: public information use in a fully automated testing environment.Animal Cognition, DOI 10.1007/s10071-011-0424-3.3. Sakai, T., Mikami, A., Tomonaga, M., Matsui, M., Suzuki, J., Hamada, Y., Tanaka, M.,Miyabe-Nishiwaki, T., Makishima, H., Nakatsukasa, M. & Matsuzawa, T. (2011).Differential prefrontal white matter development in chimpanzees and humans. CurrentBiology , 21, 1397-1402.4. Biro, D., Humle, T., Koops, K., Sousa, C., Hayashi, M. & Matsuzawa, T. (2010). Chimpanzeemothers at Bossou, Guinea carry the mummified remains of their dead infants. Current Biology,20(8), R351–352.5. Koops, K., McGrew, W. & Matsuzawa, T. (2010). Do chimpanzees (Pan troglodytes) usecleavers and anvils to fracture Treculia africana fruits? Preliminary data on a new form ofpercussive technology. Primates, 51, 175–178.6. Lonsdorf, E., Ross, S. & Matsuzawa, T. (eds.) (2010). The mind of the chimpanzee: Ecologicaland experimental perspectives. The University of Chicago Press.7. Matsuzawa, T. (2010). A trade-off theory of intelligence. In: Mareschal, D. et al. (eds.), Themaking of human concepts. Pp. 227–245, Oxford University Press.8. Miyabe-Nishiwaki, T., Kaneko, A., Nishiwaki, K., Watanabe, A., Watanabe, S., Maeda,N., Kumazaki, K., Morimoto, M., Hirokawa, R., Suzuki, J., Ito, Y., Hayashi, M., Tanaka,M., Tomonaga, M. & Matsuzawa, T. (2010). Tetraparesis resembling acute transversemyelitis in a captive chimpanzee (Pan troglodytes): Long-term care and recovery.Journal of Medical Primatology, 39, 336–346.9. Humle, T. & Matsuzawa, T. (2009). Laterality in hand use across four tool-usebehaviors among the wild chimpanzees of Bossou, Guinea, West Africa. AmericanJournal of Primatology, 70, 40–48.10. Matsuzawa, T. (2009). Symbolic representation of number in chimpanzees. CurrentOpinion in Neurobiology, 19, 92–98.4041

Invited SpeakersSensory experience-dependent reorganizationof neuronal Sensory experience-dependent circuits in the olfactory reorganization cortex ofand neuronal olfactory circuits bulb in during the olfactory postprandial cortex olfactory sleepbulb during postprandial sleepKensaku MoriDepartment of Physiology, Graduate School of Medicine, University of TokyoKensaku MoriDepartment of Physiology, Graduate School of Medicine, University of TokyoAbstract: Learning and recognition of odor cues that predict the availability of nutritiousfoods are essential for the daily life of humans and animals. During food-explorationbehavior, olfactory cortex (OC) is engaged in the processing of external odor information. Incontrast, the OC is functionally isolated from the external odor world during slow-wavesleep. However, the neuronal activity pattern in the OC and its functional roles duringslow-wave sleep are not well understood yet. In the present study, we demonstrate in freelybehaving rats that the OC repeatedly generates sharp waves (SPWs) that are accompaniedby synchronized discharges of numerous cortical neurons. The frequency of OC-SPWsincreased about 2 times during postprandial sleep compared with the sleep withoutpreceding eating. During slow-wave sleep, the olfactory bulb (OB) showed SPWs that werein synchrony with OC-SPWs, indicating that OC-SPWs drove synchronized top-down inputsto the OB.Granule cells (GCs) in the rodent OB continue to be generated in adulthood, with nearlyhalf incorporated and the remainder eliminated. Here, we show that elimination ofadult-born GCs is promoted during postprandial sleep. Deprivation of olfactory sensoryexperience in the local OB area potentiated the extent of GC elimination in that area duringpostprandial sleep. These results suggest that extensive structural reorganization of OBcircuitry occurs under the instruction of top-down inputs from OC during the postprandialsleep, reflecting sensory experience during preceding waking period.Biography:-Dept. of Physiology, School of Medicine, Gunma University,Assistant Professor (1974-1978), Lecturer (1980-1987)-Dept. of Physiology and Section of Neuroanatomy, Yale Univ. Sch. of Medicine. USAResearch Associate (1978-1980)-Dept. of Neuroscience, Osaka Bioscience Institute, Vice-Head (1987-1995)-Lab. for Neuronal Recognition Molecules, Neuronal Function Research Group,Frontier Research Program and Brain Science Institute, RIKENGroup Director and Lab. Head (1995-2000)-Dept. of Physiology, Graduate School of Medicine, University of TokyoProfessor (1999-present)Publications:1. Mori, K. and Sakano, H. (2011) How is the olfactory map formed and interpreted in themammalian brain? Annu. Rev. Neurosci. 34: 467-499.2. Yokoyama, T.K., Mochimaru, D., Murata, K., Manabe H, Kobayakawa, K., Kobayakawa,R., Sakano, H., Mori, K., and Yamaguchi M. (2011) Elimination of adult-born neurons inthe olfactory bulb is promoted during the postprandial period. Neuron 71(5):883-897.3, Manabe, H., Kusumoto-Yoshida, I., Ota, M. and Mori, K. (2011) Olfactory cortexgenerates synchronized top-down inputs to the olfactory bulb during slow-wave sleep.J. Neurosci. 31(22): 8123-8133.4, Murata, M., Imai, M., Nakanishi S., Watanabe, D., Pastan I., Kobayashi, K., Nihira T.,Mochizuki, H., Yamada, S., Mori, K. and Yamaguchi, M. (2011) Compensation of depletedneuronal subsets by new neurons in a local area of the adult olfactory bulbJ. Neurosci. 31(29): 10540-10557.5. Sakamoto, M., Imayoshi, I., Ohtsuka,T., Yamaguchi, M, Mori, K. and Kageyama, R.(2011) Continuous neurogenesis in the adult forebrain is required for innate olfactoryresponses Proc. Natl. Acad. Sci. USA 108(20): 8479-8484.6. Kikuta S., Sato, K., Kashiwadani H., Tsunoda, K., Yamasoba, T and Mori K. (2010)Neurons in the anterior olfactory nucleus pars externa detect right and left localization ofodor sources. Proc. Natl. Acad. Sci. USA 107: 12363-12368.7. Imayoshi, I., Sakamoto, M., Ohtsuka T., Takao, K., Miyakawa, T., Yamaguchi, Y., Mori,K., Ikeda, T., Itohara, S. and Kageyama, R. (2008) Long-term labeling and ablation revealrequirement of continuous neurogenesis for the structural and functional integrity of theadult forebrain. Nature Neuroscience, 11:1153-1161.8. Kobayakawa, K., Kobayakawa, R., Matsumoto, H., Oka, Y., Imai, T., Ikawa, M., Okabe,M., Ikeda, T., Itohara, S., Kikusui, T., Mori, K. and Sakano, H. (2007) Innate versuslearned odor processing in the mouse olfactory bulb Nature, 450: 503-508.9. Mori, K., Takahashi, Y.K., Igarashi, K.M. and Yamaguchi, Y. (2006) Maps of odorantmolecular features in the mammalian olfactory bulb Physiological Reviews. 86(2): 409-433.10. Murakami, M., Kashiwadani, H., Kirino, Y. and Mori, K (2005) State-dependentsensory gating in olfactory cortex Neuron 46:285-296.4243

Invited SpeakersFunctional architecture of cerebral cortexFunctional architecture of cerebral cortexKenichi OhkiDepartment of Molecular Physiology, Graduate School of Medical Sciences,Kyushu UniversityKenichi OhkiDepartment of Molecular Physiology, Graduate School of Medical Sciences, Kyushu UniversityIt has been suggested that local cortical circuits are composed of arrays of anatomicalunits that run perpendicular to the cortical surface. There are two such anatomical units,called a minicolumn and a microcolumn. A minicolumn is a one-cell-wide vertical arrayof cell bodies of neurons. A microcolumn is a group of neurons, located roughlyvertically, and their apical dendrites make a bundle in upper layers. It has beensuggested that neurons in a microcolumn send axons to specific targets, and amicrocolumn may serve as a cortical output unit (Innocenti et al., 2010), but it is stillunder debate whether these anatomical structure have any functional correlate.Biography1996 M.D. from University of Tokyo, Medical School2000 Ph.D. from University of Tokyo2000-2002 Instructor, University of Tokyo2002-2010 Research Fellow and Instructor, Harvard Medical School2010- Professor, Kyushu UniversityPublicationsK. Ohki, S. Chung, Y. H.Ch'ng, P. Kara, R. C. Reid. Functional imaging with cellularresolution reveals precise micro-architecture in visual cortex. Nature: Vol. 433: 597-603(2005).K. Ohki, S. Chung, P. Kara, M. Hubener, T. Bonhoeffer, R. C. Reid. Highly orderedarrangement of single neurons in orientation pinwheels. Nature: Vol. 442: 925-928(2006).K. Ohki, R. C. Reid. Specificity and randomness in the visual cortex. Curr. OpinionNeurobiol. Vol., 17: 401-407 (2007).We examined whether neurons that belong to either of these anatomical units share thesame function in visual processing. We obtained 3-dimensional functional maps ofmouse visual cortex with in vivo 2-photon volume imaging of calcium signal, in whicha volume (340x170x200 micron) was scanned every 0.6 seconds, using a combinationof a resonant scanner and a piezo drive. We successfully reconstructed threedimensionalfunctional maps in layer II/III of mouse visual cortex. We tested whetherneurons in a minicolumn share the same selectivity for orientation, direction, spatialfrequency, or receptive field position. Surprisingly, none of these features were sharedby neurons in a minicolumn. We also tested whether neurons in a microcolumn sharethe same selectivity, by imaging from a bundle of apical dendrites. Again, apicaldendrites of a bundle had diverse selectivity. We propose that a microcolumn receivesdiverse information to send a set of information to a specific target.This newly found motif of functional architecture suggested that individual neurons in aminicolumn or microcolumn receive highly specific and differential inputs. Indeed, theexistence of networks of specifically connected subpopulation of excitatory neurons -subnetworks - were found in rodent visual cortex, and they were related to orientationselectivity (Ho et al., 2011). We are now addressing whether there exists anydevelopmental basis of such subnetworks. I would like to discuss a possibility thatresponse selectivity of pyramidal neurons may be affected by their cell lineage.4445

Invited SpeakersA neandertal perspective on human originsA neandertal perspective on human originsSvante PääboSvante PääboMax Planck Institute for Evolutionary AnthropologyMax Planck Institute for Evolutionary AnthropologyOver the past 25 years, our laboratory has developed of techniques for extracting andanalyzing DNA from Pleistocene fossil remains. We recently produced a genomesequence of 1.3-fold genomic coverage from Neandertals, who lived in western Eurasiauntil becoming extinct around 30,000 years ago. We find that about 2.5% of the genomesof people living outside Africa derive from Neandertals, implying that interbreedingoccurred between Neandertals and the ancestors of all present-day people living outsideAfrica.We have also sequenced the genome of an ancient finger bone from DenisovaCave in southern Siberia to 1.9-fold coverage. The analysis of the sequence reveals that itdrives from a hitherto unknown group of hominins, which we call Denisovans. Thisgroup shared a common DNA ancestor with Neandertals about 650,000 years ago andwith present-day humans around 800,000 years ago. Approximately 4.8% of the genomesof people now living in Papua New Guinea and other parts of Melanesia derive fromDenisovans, suggesting interbreeding in eastern Eurasia between Denisovans andancestors of some present-day human groups.Together, these finding suggest a ‘leaky replacement’ scenario of human originsin which anatomically modern humans emerged out of Africa beginning around 1000,000years ago and received some degree of gene flow from the anatomically archaic humanpopulations in Eurasia that they ultimately replaced. The Neandertal and Denisovagenomes also allow novel genomic features that appeared and became fixed in presentdayhumans since their divergence from common ancestors with these archaic humans tobe identified, and regions likely to have been affected by positive selection in modernhumans since their divergence from a common ancestor shared with Neandertals andDenisovans to be identified. I will describe our analysis of some such candidates, as wellas our work that focuses on the evolution FOXP2 in humans, a gene involved in thedevelopment of speech and language.Svante Pääbo has developed technical approaches that allow DNA sequences from extinctcreatures such as mammoths, ground sloths and Neandertals to be determined. He also works onthe comparative genomics of humans, extinct hominins and apes, particularly the evolution ofgene activity and genetic changes that may underlie aspects of traits specific to humans such asspeech and language. In 2010, his group determined the first Neandertal genome sequence anddescribed Denisovans, a sister group of Neandertals, based on a genome sequence determinedfrom a small bone found in Siberia.Svante Pääbo holds several honorary degrees, has received several scientific prizes and is amember of numerous academies. He is currently a Director at the Max-Planck Institute forEvolutionary Anthropology in Leipzig, Germany.4647

Svante PääboSelected Scientific ArticlesPääbo, S.: Molecular cloning of ancient Egyptian mummy DNA. Nature 314: 644-645 (1985).Pääbo, S.: Ancient DNA; extraction, characterization, molecular cloning and enzymaticamplification. Proc. Natl. Acad. Sci. USA 86: 1939-1943 (1989).Krings, M., Stone, A., Schmitz, R.W., Krainitzki, H., Stoneking, M., and Pääbo, S.: NeandertalDNA sequences and the origin of modern humans. Cell 90: 19-30 (1997).Green, R.E., Krause, J., Ptak, S.E., Briggs, A.W., Ronan, M.T., Simons, J.F., Du, L., Egholm, M.,Rothberg, J.M., Paunovic, M., and Pääbo, S.: Analysis of one million base pairs of NeanderthalDNA. Nature 444: 330-36 (2006).Krause, J., Orlando, L., Serre, D., Viola, B., Prüfer, K., Richards, M.P., Hublin, J.-J., Hänni, C.,Derevianko, A.P., and Pääbo, S.: Neanderthals in central Asia and Siberia. Nature 449: 902-904(2007).Green, R.E., Malaspinas, A.-S., Krause, J., Briggs, A.W., Johnson, P.L.F., Uhler, C., Meyer, M.,Good, J.M., Maricic, T., Stenzel, U., Prüfer, K., Siebauer, M., Burbano, H.A., Ronan, M.,Rothberg, J.M., Egholm, M., Rudan, P., Brajković, D., Kućan, Ž., Gušić, I., Wikström, M.,Laakkonen, L., Kelso, J., Slatkin, M., and Pääbo, S.: A complete Neandertal mitochondrialgenome sequence determined by high-throughput sequencing. Cell 134: 416-426 (2008).Briggs, A., J.M. Good, R.E. Green, J. Krause, T. Maricic, U. Stenzel, C. Lalueza-Fox, P. Rudan,D. Brajković, Ž. Kućan, I. Gušić, R. Schmitz, V.B. Doronichev, L.V.Golovanova, M. de laRasilla, J. Fortea, A. Rosas and S. Pääbo: Targeted retrieval and analysis of five NeandertalmtDNA genomes. Science 325, 318-321 (2009).Krause, J., Fu, Q., Good, J.M., Viola, B., Shunkov, M.V., Derevianko, A.P., and Pääbo, S.: Thecomplete mtDNA genome of an unknown hominin from Southern Siberia. Nature 464: 894- 897(2010).Green, R.E., Krause, J., Briggs, A.W., Maricic, T., Stenzel, U., Kircher, M., Patterson, N., Li, H.,Zhai, W., Fritz, M.H-Y., Hansen, N.F., Durand, E.Y., Malaspinas, A.-S., Jensen, J.D., Marques-Bonet, T., Alkan, C., Prufer, K., Meyer, M., Burbano, H.A., Good, J.M., Schultz, R., Aximu-Petri, A., Butthof, A., Hober, B., Hoffner, B., Siegemund, M., Weihmann, A., Nusbaum, C.,Lander, E.S., Russ, C., Novod, N., Affourtit, J., Egholm, M., Verna, C., Rudan, P., Brajkovic, D.,Kucan, Ž., Gušic, I., Doronichev, V.B., Golovanova, L.V., Lalueza-Fox, C., de la Rasilla, M.,Fortea, J., Rosas, A., Schmitz, R.W., Johnson, P.L.F., Eichler, E.E., Falush, D., Birney, E.,Mullikin, J.C., Slatkin, M., Nielsen, R., Kelso, J., Lachmann, M., Reich, D., and Pääbo, S.: Adraft sequence of the Neandertal genome. Science 328: 710-22 (2010).Reich, D., Green, R.E., Kircher, M., Krause, J., Patterson, N., Durand, E.Y., Viola, B., Briggs,A.W., Stenzel, U., Johnson, P.L.F., Maricic, T., Good, J.M., Marques-Bonet, T., Alkan, C., Fu,Q., Mallick, S., Li, H., Meyer, M., Eichler, E.E., Stoneking, M., Richards, M., Talamo, S.,Shunkov, M.V., Derevianko, A.P., Hublin, J.-J., Kelso, J., Slatkin, M., and Pääbo, S.: Genetichistory of an archaic hominin group from Denisova Cave in Siberia. Nature 468:1053-1060(2010).48

Invited SpeakersCircuit mechanisms Mechanisms for for Perceptual perceptual Memory memory of theof Temporal the temporal Sequence sequence and Time and Intervals time of intervals Sensoryof sensory eventsEventsMu-ming PooUniversity of California, Berkeley, USAInstitute of Neuroscience, Chinese Academy of SciencesMu-ming PooUniversity of California, Berkeley, USAInstitute of Neuroscience, Chinese Academy of SciencesSix decades after the publication of “The Organization of Behavior” by Donald Hebb, theneural circuit basis of perceptual memory remain an unsolved mystery. Hebb postulatedthat the first step in perceptual memory in the brain is the formation of an experiencespecificassembly of neurons, and experience-induced persistent “reverberatory”correlated activity facilitates the formation of the cell assembly by selectivelystrengthening synaptic connections among these neurons. I will review our recent effortsin search of the circuit mechanism for perceptual memory of temporal sequence and timeintervals of sensory events. In the rodent primary visual cortex, we have obtainedevidence that spike timing-dependent plasticity (STDP) of intracortical connections mayprovide a mechanism for short-term storage of sequence information associated with adirectional moving object. In the optic tectum of zebrafish larvae, we found that anensemble of tectal neurons could store the information of the time interval (on the orderof seconds) via rhythmic correlated spiking activities among the specific ensemble.Furthermore, unlike long-term potentiation/depression (LTP/LTD) found in slicepreparations, synaptic modification induced by a single episode of repetitive correlatedpre- and postsynaptic spiking is quickly erased by the high-level spontaneous activity invivo, but repeated episodes of the same total number of spikes resulted in stableLTP/LTD. This suggests that long-term perceptual memory of sensory experiencerequires spaced pattern of sensory activities.Recent Publications:Engart, F., Tao, H., Zhang, L., and M-m. Poo. Moving stimuli induces directionsensitiveresponses of developing tectal neurons. Nature, 419, 470-474 (2002)Zhou, Q., Tao, H., and M-m. Poo. Reversal and stabilization of synaptic modifications ina developing visual system. Science 300, 1953-7 (2003)Kobayashi, K. & M-m. Poo. Spike train timing dependent associative synapticmodification in CA3 hippocampal pyramidal neurons. Neuron, 41: 445-54 (2004)Liu, Q-s., Pu, L. & Poo, M-m. Repeated cocaine exposure facilitates LTP induction inmidbrain dopamine neurons. Nature 437:1027-31 (2005)Dan, Y. & Poo, M-m. Spike timing-dependent plasticity: from synapse to perception.Physiol. Rev. 86:1033-48 (2006).Sumbre, G., Muto, A., Baier H., Poo M-m. Entrained rhythmic activities of neuronalensembles as perceptual memory of time interval.. Nature 456:102-6 (2008)Li CY, Poo M-m., Dan Y. Burst spiking of a single cortical neuron modifies global brainstate. Science. 324: 643-6 (2009).Du, J.L., Wei, H.P., Wang, Z.R., Wong, S.T., Poo, M-m. Long-range retrograde spreadof LTP and LTD from optic tectum to retina. Proc. Natl. Acad. Sci. U S A. 106:18890-6(2009).Biographic SketchMu-ming Poo received his B.S. in physics from Tsinghua University in Taiwan in 1970,and Ph. D in biophysics from Johns Hopkins University in 1974. He had served on thefaculty of University of California at Irvine, Yale University, Columbia University, andUniversity of California at San Diego, before joining University of California, Berkeleyin 2000, where he is currently Paul Licht Distinguished Professor in the Department ofMolecular and Cell Biology. Since 1999, he also served as the Director of Institute ofNeuroscience, Chinese Academy of Sciences in Shanghai. Poo’s research interests coveraxon guidance, neuronal polarity formation, synaptic plasticity, and neural circuitfunctions. He received Javitz Neuroscience Investigator Award of NIH (1998), AmeritecPrize (2001), Docteur Honoris Causa from Ecole Normale Supérieure, Paris (2003), P. R.China International Science & Technology Cooperation Award (2005), and QiushiDistinguished Scientist ward (2010). He is a fellow of AAAS, and a member of AcademiaSinica (Taiwan) and National Academy of Sciences (US).5051

Invited SpeakersEmergence of novel chemosensors:from the immune to the olfactory systemEmergence of novel chemosensors: from the immuneto the olfactory systemIvan RodriguezIvan RodriguezDepartment of Genetics and Evolution, University of Geneva, SwitzerlandDepartment of Genetics and Evolution, University of Geneva, SwitzerlandFormyl peptide receptor (FPR) genes are found in all mammals. They areexpressed in immune cells and recognize disease and pathogen-relatedmolecules. Recently, in some rodent species, gene duplication eventsfollowed by gene cluster invasion led to the intermingling of vomeronasalreceptor and FPR genes. This accident correlates with a drastically differentexpression pattern of most FPRs in these species: their transcription is absentfrom immune cells, and is restricted to sensory neurons of the vomeronasalorgan. The peculiar agonist profile of these vomeronasal FPR receptors, andtheir maintenance in multiple rodent species, suggest that this acquisition maybe of selective advantage. Taken together, this rodent-specific chemosensorytool may represent a clean example of evolutionary novelty, resulting fromgenomic landscape alterations that led to the hijacking by FPR genes of cisregulatory sequences from neighbouring genes.52

BiographyInvited SpeakersNeuronal identity and circuit formationin the mouse olfactory systemNeuronal identity and circuit formation in the mouseolfactory systemHitoshi SakanoUniversity of TokyoHitoshi SakanoUniversity of TokyoAbstractIn the mouse olfactory system, much of axon wiring in neural map formation occursautonomously by olfactory sensory neurons (OSNs). Axonal projection along thedorsal-ventral (D-V) axis is regulated by positional information of OSNs within the olfactoryepithelium (OE). Axon guidance molecules, such as Neuropilin-2 (Nrp2) and Semaphorin-3F(Sema3F) that are expressed by OSNs in a complementary manner, determine D-V positioningof glomeruli. Sema3F secreted by early^arriving dorsal-zone axons repel Nrp2-positivelate-arriving axons.Unlike the projection along the D-V axis, anterior-posterior (A-P) positioning of glomeruliis independent of positional information of OSNs in the OE. Instead, OR molecules regulatethe expression levels of axon guidance molecules, e.g., Nrp1 and Sema3A, using OR-derivedcAMP signals. How is it, then, that cAMP signal levels are uniquely determined by each ORspecies? Many G-protein coupled receptors (GPCRs) are known to have two differentconformations, active and inactive, and spontaneously transit between the two, generating thebasal activity in the absence of agonists. We assume that the OR-derived basal activityparticipates in the olfactory map formation.Due to the difficulty of expressing membrane ORs in vitro, it has not been easy to study thepossible role of OR basal activity in the axonal projection of OSNs. 2-adrenergic receptor(2-AR) is known to share many functional similarities with OR molecules and substitute ORsfor OR-instructed OSN projection. Taking advantage of these observations, we have analyzedaxonal projection of OSNs that express the mutant-type 2-AR with the altered levels of basalactivity. We have found that the basal activity mutants of 2-AR alter expression levels ofaxon guidance molecules, e.g., Nrp1 and Sema3A, and change glomerular locations along theA-P axis in the OB.In rodents, axon-derived guidance molecules alone could organize an olfactory map byaxon-axon interactions of OSNs even in the absence of the target OB. However, the mapneeds to be properly connected with second-order neurons, mitral/tufted (M/T) cells, to makethe olfactory circuit functional. Here we report that Sema3F, a repulsive ligand to Nrp2,which is secreted by dorsal OSN axons, guides both Nrp2 + OSN axons and their partner Nrp2 +M/T cells to the ventral region of the OB. This coordinated guidance is an important processfor proper alignment and synapse formation of OSN axons with M/T cells during olfactorydevelopment.Hitoshi SakanoDepartment of Biophysics and Biochemistry, Graduate School of Science, University of TokyoBiographyDr. Sakano received his Ph.D. degree in 1976 from Kyoto University under thesupervision of Prof. Yoshiro Shimura. For his theses work, Dr. Sakano investigatedtRNA processing/splicing by isolating and characterizing the temperature-sensitivemutants of E coli, which were mapped at two different genetic loci. It was later foundthat one locus codes for RNaseP protein and the other for the RNA component of RNaseP,a ribozyme. This discovery served as a genetic 54 proof for Dr. Altman’s biochemicalstudies on RNaseP that won him the Nobel Prize in 1989.Dr. Sakano, then, spent one year and a half as a postdoc with Prof. John Abelson atDr. Sakano received his Ph.D. degree in 1976 from Kyoto University under thesupervision of Prof. Yoshiro Shimura. For his theses work, Dr. Sakano investigatedtRNA processing/splicing by isolating and characterizing the temperature-sensitivemutants of E coli, which were mapped at two different genetic loci. It was later foundthat one locus codes for RNaseP protein and the other for the RNA component of RNaseP,a ribozyme. This discovery served as a genetic proof for Dr. Altman’s biochemicalstudies on RNaseP that won him the Nobel Prize in 1989.Dr. Sakano, then, spent one year and a half as a postdoc with Prof. John Abelson atUCSD studying yeast tRNA splicing. From 1978 to 1981, Dr. Sakano worked with Prof.Susumu Tonegawa on immunoglobulin (Ig) genes to solve the problem of antibodydiversity. He published five Nature article papers, providing the evidence forcombinatorial and junctional diversification of antibody genes.Once independent at UC Berkeley as Assistant Professor of Immunology in 1982, Dr.Sakano continued to work on Ig gene rearrangement and was promoted to Full Professorin 1992. Dr. Sakano relocated to the University of Tokyo in 1996, changing his researchfield to Neuroscience. Since then, he has been studying axon wiring and neural mapformation in the mouse olfactory system.Selected Publications (last 5 yeas)Imai, T., Suzuki, M., and Sakano, H.: Odorant receptor-derived cAMP signals direct axonaltargeting. Science 314, 657-661 (2006).Serizawa, S., Miyamichi, K., Takeuchi, H., Yamagishi, Y., Suzuki, M., and Sakano, H.: Aneuronal identity code for the odorant receptor-specific and activity-dependent axon sorting.Cell 127, 1057-1069 (2006).Nagawa, F., Kishishita, N., Shimizu, K., Hirose, S., Miyoshi, M., Nezu, J., Nishimura, T.,Nishizumi, H., Takahashi, Y., Hasimoto, S., Takeuchi, M., Miyajima, A., Takemori, T.,Otsuka, A.J., and Sakano, H.: Antigen receptor genes of the agnathan lamprey areassembled by a process involving copy choice. Nature Immunol. 8, 206-213 (2007).Kobayakawa, K., Kobayakawa, R., Matsumoto, H., Oka, Y., Imai, T., Ikawa, M., Okabe, M.,Ikeda, T., Itohara, S., Kikusui, T., Mori, K., and Sakano, H.: Innate versus learned odorprocessing in the mouse olfactory bulb. Nature 450, 503-508 (2007).Nishizumi, H., Kumasaka, K., Inoue, N., Nakashima, A., and Sakano, H.: Deletion of thecore-H region in mice abolishes the expression of three proximal odorant receptor genes in cis.Proc. Natl. Acad. Sci., USA 104, 20067-20072 (2007).Imai, T., Yamazaki, T., Kobayakawa, R., Kobayakawa, K., Takeuchi, H., Abe, T., Suzuki, M.,and Sakano, H.: Pre-target axon sorting establishes the neural map topography. Science 325,585-590 (2009).Takeuchi, H., Inokuchi, K., Aoki, M., Suto, F., Tsuboi, A., Matsuda, I., Suzuki, M., Aiba, A.,Serizawa, S., Yoshihara, Y., Fujisawa, H., and Sakano, H.: Sequential arrival and gradedsecretion of Sema3F by olfactory neuron axons specify map topography at the bulb. Cell141, 1056-1067 (2010).Sakano, H.: Neural map formation in the mouse olfactory system. Neuron 67, 530-542(2010).Tsuboi, A., Imai., T., Kato, H.K., Matsumoto, H., Igarashi, K.M., Suzuki, M., Mori, K., andSakano, H.: Two highly homologous mouse odorant receptors encoded by tandemly-linkedMOR29A and MOR29B genes respond differently to phenyl ethers. Eur. J. Neurosci. 33,205-213 (2011).Mori, K. and Sakano, H.: How is the olfactory map formed and interpreted in the mammalianbrain? Ann. Rev. Neurosci. 34, 465-497 (2011).55

Invited SpeakersOlfactory white: odorant mixtures containingmany components converge towardsa common perceptNoam SobelDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, IsraelBrief Biography:Noam completed a PhD in Neuroscience at Stanford University in 1999. Following abrief postdoctoral stint as a Hellen Hay Whitney Fellow at CalTech division ofBiology, he joined the faculty of the Wills Neuroscience Center at UC Berkeley, as anAssistant Professor (2001), and later Associate Professor (2005). In 2006 he joinedthe Department of Neurobiology at the Weizmann Institute in Rehovot, Israel, wherehe is Professor of Neurobiology. Noam’s lab studies human olfaction.10 Selected Recent publications:Olfactory white: odorant mixtures containing manycomponents converge towards a common perceptNoam SobelDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, IsraelAbstract:In vision, mixtures that combine all visible wavelengths, each at equal intensity, areperceived as white. In audition, sounds that combine all heard frequencies, each atequal amplitude, are perceived as a hum termed white noise. Here we found a similarperceptual phenomenon in olfaction. As we added equal-intensity components thatspanned olfactory space to each of two mixtures, the mixtures became more similar toeach other, despite not sharing a single component in common. Remarkably, from~30 components, all mixtures began to smell similar, obtaining a quality we calledolfactory white. Such early perceptual morphing poses computational boundaries forthe olfactory system, and like auditory white noise, may find its way into everydaylife applications.Hadas Lapid, Sagit Shushan, Anton Plotkin, Hillary Voet, Yehudah Roth, ThomasHummel, Elad Schneidman & Noam Sobel. (2011) Neural activity at the humanolfactory epithelium reflects olfactory perception. Nature Neuroscience. 14(11):1455- 1461Gelstein S, Yeshurun Y, Rozenkrantz L, Shushan S, Frumin I, Roth Y, Sobel N.(2011) Human tears contain a chemosignal. Science. 331(6014):226-30.Plotkin A, Sela L, Weissbrod A, Kahana R, Haviv L, Yeshurun Y, Soroker N, SobelN. (2010) Sniffing enables communication and environmental control for the severelydisabled. Proc Natl Acad Sci U S A. 10;107(32):14413-8.Sela L, Sobel N. (2010). Human olfaction: a constant state of change-blindness.Experimental Brain Research 205(1):13-29.Haddad R, Weiss T, Khan R, Nadler B, Mandairon N, Bensafi M, Schneidman E,Sobel N. (2010). Global features of neural activity in the olfactory system form aparallel code that predicts olfactory behavior and perception. Journal of Neuroscience30(27):9017-26.Haddad R, Medhanie A, Roth Y, Harel D, Sobel N. (2010). Predicting odorpleasantness with an electronic nose. PLoS Computational Biology 6(4):e1000740.Yaara Yeshurun and Noam Sobel (2009). An Odor is Not Worth a Thousand Words:From Multidimensional Odors to Unidimensional Odor Objects. Annual Review ofPsychology. 2010;61:219-41.Haddad R, Lapid H, Harel D, Sobel N. (2008). Measuring Smells. Curr OpinNeurobiol. Oct 3. 18(4):438-44.Haddad R, Khan R, Takahashi YK, Mori K, Harel D, Sobel N. (2008) A metric forodorant comparison. Nature Methods. 5(5):425-9.Khan RM, Luk CH, Flinker A, Aggarwal A, Lapid H, Haddad R, Sobel N. (2007)Predicting odor pleasantness from odorant structure: pleasantness as a reflection ofthe physical world. J Neurosci. 27(37):10015-23.5657

Invited SpeakersActivity-dependent neurotransmitterrespecification: novel plasticityActivity-dependent neurotransmitter respecification: novelplasticityNicholas C. SpitzerNeurobiology Section, Center for Neural Circuits & Behavior, Division of Biological Sciences,Kavli Institute for Brain and Mind, University of California, San DiegoNicholas C. SpitzerNeurobiology Section, Center for Neural Circuits & Behavior, Division of BiologicalSciences, Kavli Institute for Brain and Mind, University of California, San DiegoEver since the discovery of chemical synaptic transmission we have commonlyunderstood that the identity of neurotransmitter molecules that neurons use to signal toother neurons and target cells is fixed and invariant throughout life. However our recentstudies have demonstrated that sensory stimuli such as light or odorants respecifytransmitter expression during development of the amphibian brain. We now report thatadult rats subjected to different photoperiods show increases or decreases in thenumber of neurons expressing dopamine in hypothalamic nuclei involved in response tostress, challenging the concept of neurotransmitter stability in the mature brain..We hypothesized that changes in photoperiod observed seasonally at high latitudespromote changes in the number of dopaminergic neurons in the adult mammalianhypothalamus via activation of the retino-hypothalamic projection. We furtherhypothesized that such changes in the number of dopaminergic neurons producechanges in behavior.We find that one-week exposure to long day-short night or short day-long nightstimulation produces 20-100% decreases and increases, respectively, in the number ofdopaminergic local interneurons in the lateral preoptic area (LPO), the paraventricularnucleus (PaVN) and the periventricular nucleus (PeVN), assessed by stereologicalscoring of tyrosine hydroxylase and dopamine immunoreactivity. BrdU labeling indicatesthat adult neurogenesis is absent in these nuclei. Fluorescent false neurotransmitter511 is taken up by and released from brain slices in response to depolarization, inproportion to the number of dopaminergic neurons, indicating that the changes innumbers of dopaminergic neurons are functional. Strikingly, photoperiod-dependentincreases and decreases in numbers of dopaminergic neurons are accompanied byreciprocal decreases and increases in numbers of local interneurons expressingsomatostatin in the PaVN and PeVN.Animals’ stress-response behavior was analyzed with the elevated plus maze and theforced swim test. Rats exposed to short day-long night stimulation spend more time inthe open arm of the maze and more time swimming than their counterparts exposed tolong day-short night stimulation. Stereotactic injection of 6-OHDA ablating PaVN andLPO neurons suppresses this behavioral confidence. Subsequent short-day-long nightstimulation leads to the appearance of newly dopaminergic neurons, with recovery ofconfident behavior in response to stress. This behavior is lost following localintroduction of dopamine receptor antagonists, indicating the physiological contributionof the newly dopaminergic neurons. Demonstration of activity-dependent transmitterswitching in the adult mammalian brain identifies a novel form of plasticity.Supported by a grant from the Ellison Medical Foundation.Nicholas C. Spitzer is Distinguished Professor of Neurobiology and Co-Director of theKavli Institute for Brain and Mind (KIBM) at the University of California, San Diego. Hereceived his B.A. and Ph.D. at Harvard University. After postdoctoral work at Harvardand University College London he joined the UC San Diego faculty in 1972. He hasserved on several NIH study sections, as a member of the NIH NINDS Council and as aTrustee of the Grass Foundation. He is Editor-in-Chief of BrainFacts.org, a Fellow ofthe American Association for the Advancement of Science and a Member of theAmerican Academy of Arts and Sciences.Borodinsky, L.N., Root, C.M., Cronin, J.A., Sann, S.B., Gu, X. and Spitzer, N.C. (2004)Activity-dependent homeostatic specification of transmitter expression in embryonicneurons. Nature 429: 523-530.Borodinsky, L.N. and Spitzer, N.C. (2007) Activity-dependent neurotransmitter-receptormatching at the neuromuscular junction. Proc. Natl. Acad. Sci. 104: 335-340.Dulcis, D. and Spitzer, N.C. (2008) Illumination controls dopaminergic differentiationregulating behavior. Nature 456: 195-201.Marek, K.W., Kurtz, L.M. and Spitzer, N.C. (2010) cJun integrates calcium spike activityand tlx3 expression to regulate neurotransmitter specification. Nature Neurosci. 13:944-950.Demarque, M. and Spitzer, N.C. (2010) Activity-dependent expression of Lmx1bregulates specification of serotonergic neurons modulating swimming behavior. Neuron67: 321-334.Velázquez-Ulloa, N.A., Spitzer, N.C. and Dulcis, D. (2011) Context-dependentdopamine specification by calcium activity across the central nervous system. J.Neurosci. 31: 78-88.Nicol, X., Hong, K.P. and Spitzer, N.C. (2011) Spatial and temporal second messengercodes for growth cone turning. Proc. Nat. Acad. Sci. USA. 108: 13776-13781.5859

Invited SpeakersDiverse coding logicto encode olfactory-mediated behaviorDiverse coding logic to encode olfactory-mediated behaviorLisa StowersThe Scripps Research Institute, Department of Cell BiologyLisa StowersThe Scripps Research Institute, Department of Cell BiologyDr. Stowers received her PhD in Molecular and Cellular Biology from Harvard University in 1997.She did post-doctoral training with Catherine Dulac at Harvard University where she studied therole of olfaction to guide stereotyped behavior. In 2002 she established her own group at TheScripps Research Institute where she is now an associate professor in the department of cellbiology studying the sensory logic of innate behavior.Flanagan KA, Webb W, Stowers L. Analysis of Male Pheromones That Accelerate FemaleReproductive Organ Development. 2011 PLoS ONE 6(2): e16660.doi:10.1371/journal.pone.0016660The coding logic of sensory information detected by the vomeronasal organ has not beenidentified. Sensory information can be encoded either by 1) labeled lines in which a sensoryinput generates a precise outcome or 2) across neuron patterns by which the ensemble ofdetected sensory cues code variable information. We have generated recombinant variants ofthe large family of major urinary protein (MUP) ligands and used them each to stimulate VNOneurons and determine their corresponding behavioral output. We find that, Mups are sufficientto generate two different behaviors when detected by males; innate territorial aggression andcountermarking. Interestingly, the VNO appears to utilize a different coding strategy in responseto Mups for each of these behavioral outputs. Of the tested repertoire of Mups, only two areeach sufficient to activate a program of aggressive behavior. The response to these preciseMups appears to be genetically determined since mice that have not previously experiencedthese ligands generate aggression upon detection. In contrast, we find that all tested Mups areeach individually sufficient to initiate countermarking. However, the behavior is dependent uponthe entire repertoire of Mups in the environment as well as the history of Mups that havepreviously been detected. This behavior shows hallmarks of neuron pattern coding. Theseexperiments reveal that the VNO can generate both dedicated and variable behavior from thesame ligand, creating a system to detect and respond to an immense amount of chemosensorycues.Stowers, L., & Logan, D.W., Sexual dimorphism in olfactory signaling. 2010 Curr Opin Neurobiol10.1016/j.conb.2010.08.015.Papes, F, Logan, DW, & Stowers, L. The vomeronasal organ mediates interspecies defensivebehaviors through detection of protein pheromone homologs. 2010, Cell, 141, 692-703.Stowers, L., & Logan, D.W., Olfactory mechanisms of stereotyped behavior: on the scent ofspecialized circuits. 2010 Curr Opin Neurobiol 20:274-280.Barros C.S, Calabrese , B., Chamero, P., Roberts A.J., Korzus, E.J., Lloyd, K., Stowers, L.,Mayford, M., Halpain, S., and Müller, U. Impaired maturation of dendritic spines withoutdisorganization of cortical cell layers in mice lacking NRG1/ErbB signaling in the CNS. 2009,PNAS, 106:4507-4512.Logan, DW, Marton, TF, & Stowers, L. Species specificity in Major Urinary Proteins by parallelevolution. 2008 PLoS ONE 3:e3280Chamero, P, Marton, T.F., Logan, D.W., Flanagan, K, Cruz, J., Saghatelian, A., Cravatt, B.F., &Stowers, L. Identification of protein pheromones that promote aggressive behavior. 2007,Nature 450: 899-902.Stowers, L. and Marton, T. What is a pheromone? Mammalian pheromones reconsidered. 2005Neuron 46:1-5.Loconto, J, Papes, F, Chang, E, Stowers, L, Jones, EP, Takada, T, Kumanovics, A, FischerLindahl, K, Dulac, C , Functional Expression of Murine V2R Pheromone Receptors InvolvesSelective Association with the M10 and M1 Families of MHC Class Ib Molecules. 2003 Cell112:607-618.Stowers L, Holy TE, Meister M, Dulac C, & Koentges G. Gender discrimination and male-maleaggression are abolished in the mouse TRP2-/- mutant. 2002 Science. 295:1493-1500.6061

Enhancement of activity and Invited plasticity Speakers in visual cortexEnhancement of activity and plasticityin visual cortexMichael P. StrykerUniversity of California, San FranciscoMichael P. StrykerUniversity of California, San FranciscoActivity-dependent plasticity of binocular responses in mouse visual cortex during a criticalperiod in early life takes place in several stages that are temporally and mechanistically distinct.Occlusion of one eye initially causes a loss of response to the deprived eye dependent on calciumsignaling, which is followed by a homeostatic synaptic scaling up of the responses to the open eye thatdepends on signaling through tumor necrosis factor alpha (Kaneko et al, Neuron 2008a). Theseprocesses require adequate levels of inhibitory signaling. Neither of these stages of plasticity, however,requires neurotrophin signaling, but the subsequent recovery of normal responses after re-opening thedeprived eye does (Kaneko et al, Nature Neurosci 2008b). Responses of neurons in the visual cortexbecome larger by nearly a factor of 3 during locomotion (Niell & Stryker, Neuron 2010), suggesting apossible mechanism for the many earlier reports of effects of enriched environments on braindevelopment and plasticity.We have explored several means for enhancing plasticity in developing and adult visual cortex,including the enhancement of activity by locomotion (Kaneko poster, this meeting), the enhancement ofpresynaptic function through expression of a constitutively active H-ras transgene (Kaneko et al, PNAS2010), and the augmentation of inhibitory circuitry by the transplantation of embryonic inhibitoryneurons (Southwell et al, Science 2010). The findings suggest that at least two pathways that can affectall of these plasticity mechanisms.62

Invited SpeakersFunctional division among prefrontal areasin macaque monkeysFunctional division among prefrontal areas in macaquemonkeysKeiji TanakaCognitive Brain Mapping Laboratory, RIKEN Brain Science InstituteKeiji TanakaCognitive Brain Mapping Laboratory, RIKEN Brain Science InstituteThe neural circuitries in the prefrontal cortex are thought to be critical for the flexiblecontrol of behavior in primates, but the mechanisms remain largely unknown. Because theprefrontal cortex is composed of multiple areas each with unique anatomical connections withother brain sites, we expect that the comparison of functional roles among the prefrontalsubareas would help disentangle the processes of flexible behavioral control.Application of previously learned behavioral rules beyond simple stimulus-action oraction-outcome associations is often necessary in goal-directed behavior, and the currentlyrelevant rule is often not directly indicated by sensory cues. The Wisconsin Card Sorting Test(WCST) mimics such a situation. We have developed an animal version of WCST and trainedmonkeys with the task. The monkey selected one of the three test stimuli by matching it withthe sample stimulus in color or in shape. The matching rule was constant within a block oftrials, but changed between blocks without giving any notice to the monkey. There was nocue to indicate the currently relevant rule: the monkey had to find the currently relevant ruleonly based on rewards given after correct responses and error signals given after erroneousresponses. Lesion of the principal sulcus region (PS), the orbitofrontal region (OFC) and theanterior cingulated sulcus region (ACS) resulted in significant degradation of the overallperformance of the monkeys. Further analyses of the monkeys’ performance in the task and inother probe tests showed that the reasons of the degradation were different. Only the PSlesion impaired maintenance of abstract rules in working memory; only the OFC lesionimpaired rapid reward-based updating of rule value; and the ACS lesion impaired activereference to the content of the rule working memory.These results show that the prefrontal subareas contribute to the flexible control ofbehavior by playing individually specific functional roles.Keiji Tanaka, Ph. D.Cognitive Brain Mapping Laboratory,RIKEN Brain Science Institute2-1 Hirosawa, Wako, Saitama 351-0198, JapanBrief biographyEducation and DegreeB. Sci Department of Biophysical Engineering, Faculty of Engineering Science, OsakaUniversity, 1973M. Sci Department of Biophysical Engineering, Faculty of Engineering Science, OsakaUniversity, 1975Ph. D. Faculty of Medicine, University of Tokyo, 1983 (by dissertation)Appointments1975-1989 Researcher, NHK Science and Technical Research Laboratories1989-1996 Head, Laboratory for Neural Information Processing, Frontier ResearchProgram, RIKEN1992-1997 Head, Information Science Laboratory, RIKEN1997-present Head, Cognitive Brain Mapping Laboratory, RIKEN Brain Science Institute2003-present Deputy Director, RIKEN Brain Science Institute (2008-2009, ActingDirector)List of recent publications1) Matsumoto, K., Suzuki, W., Tanaka, K. (2003) Neuronal correlates of goal-based motorselection in the prefrontal cortex. Science 301: 229-232.2) Wang, G., Obama, S., Yamashita, W., Sugihara, T., Tanaka, K. (2005) Prier experience ofrotation is not required for recognizing objects seen from different angles. Nature Neurosci. 8:1568-1575.3) Mansouri, F. A., Matsumoto, K., Tanaka, K. (2006) Prefrontal cell activities related tomonkeys’ success and failure in adapting to rule changes in a Wisconsin Card Sorting Test(WCST) analog. J. Neurosci. 26: 2745-2756.4) Suzuki, W., Matsumoto, K., Tanaka, K. (2006) Neuronal responses to object images in themacaque inferotemporal cortex at different stimulus discrimination levels. J. Neurosci. 26:10524-10535.5) Matsumoto, M. Matsumoto, K, Abe, H., Tanaka, K. (2007) Medial Prefrontal Cell ActivitySignaling Prediction Errors of Action Values. Nature Neurosci. 10: 647-656.6) Kiani, R., Esteky, H., Mirpour , K., Tanaka , K. (2007) Object Category Structure inResponse Patterns of Neuronal Population in Monkey Inferior Temporal Cortex. J.Neurophysiol. 97: 4296-4309.7) Sun, P., Ueno, K., Waggoner, R. A., Gardner, J. L., Tanaka, K., Cheng, K. (2007) Atemporal frequency–dependent functional architecture in human V1 revealed by highresolutionfMRI. Nature Neurosci. 10, 1404-1406.8) Mansouri, F.A., Buckley, M.J., Tanaka, K. (2007) Mnemonic function of lateral prefrontalcortex in conflict-induced behavioral adjustment. Science 318: 987-990.9) Buckley MJ, Mansouri FA, Hoda H, Mahboubi M, Browning PFG, Kwok SC, Phillips A,Tanaka K (2009) Dissociable components of rule-guided behavior depend on distinct medialand prefrontal regions. Science 325: 52-58.10) Wan X, Nakatani H, Ueno K, Asamizuya T, Cheng K, Tanaka K (2011) The neural basisof intuitive best next-move generation in board game experts. Science 331: 341-346.6465

Invited SpeakersNarrowly-tuned chemosensory receptionfor pheromone food and signals pheromone signalsNarrowly-tuned chemosensory reception for food andof neural circuitries that are designed to send the specific information, leading to the attractivebehavior Associate in Professor, insect. A Department pheromone of or Integrated food odorant Biosciences, that is crucial The for University survival of or Tokyo, mating 2009- is oftendetected Professor, by Department a specific of chemosensory Applied Biological receptor Chemistry, expressed The by University peripheral of Tokyo; olfactory RH sensory Wrightneurons. Award 2006; Japan Academy Medal 2010Kazushige TouharaThe University of TokyoAbstract:Kazushige TouharaThe University of TokyoPheromones elicit an instinctive behavior or neuroendocrine change in different individualswithin the same species, and thus, are important chemosignals for maintaining the species. Inmice, we discovered a male-specific peptide, named exocrine gland-secreting peptide 1 (ESP1),that was released into tear fluids from the extraorbital lacrimal gland. ESP1 turned out to be asex pheromone that enhanced female sexual receptive behavior upon male mounting, leading tothe successful copulation. Although ESP1 secretion was observed in only a small subset ofinbred strains and closed colony, a large amount of ESP1 was detected in male tears of almostall wild-derived mouse strains, suggesting that ESP1 plays an important role in sexual behaviorin nature. Moreover, we revealed the molecular mechanisms and the neural pathway involvedin decoding the ESP1 signal in the vomeronasal system. ESP1 is recognized by a specificvomeronasal receptor V2Rp5 expressed in vomeronasal sensory neurons, resulting in signaltransmission to the amygdaloid and hypothalamic nuclei via the accessory olfactory bulb in asexually dimorphic fashion. Furthermore, we found that ESP1-induced neural activation andbehavior were diminished in the V2Rp5 knock-out mice. The ESP1-signal processing in thevomeronasal system appears to be mediated by the selective neural pathway via the V2Rp5.This study provides the functional link between a sex peptide pheromone and a behavioraloutput via a selective neural pathway activated by a specific receptor in the vomeronasal system.In this talk, I will also describe other examples of neural circuitries that are designed to send thespecific information, leading to the attractive behavior in insect. A pheromone or food odorantthat is crucial for survival or mating is often detected by a specific chemosensory receptorexpressed by peripheral olfactory sensory neurons.Biography:B.Sc. 1989 (The University of Tokyo), Ph.D. 1993 (State University of New York at StonyBrook), 1993-1995 Postdoctoral fellow, Duke University Medical Center (with Dr. Robert J.Lefkowitz), 1995-1998 Assistant Professor, Institute for Brain Research, The University ofTokyo, 1998-99 Assistant Professor, Biosignal Research Center, Kobe University, 1999-2009A list of recent publications:1. Sato, K., Tanaka, K., *Touhara K. Sugar-regulated cation channel formed by an insectgustatory receptor. Proc. Natl. Acad. Sci. U.S.A. 108, 11680-11685 (2011)2. Haga S, Hattori T, Sato T, Sato K, Matsuda S, Kobayakawa R, Sakano H, Yoshihara Y,Kikusui T, T, *Touhara K. K. The The male male mouse mouse pheromone pheromone ESP1 enhances ESP1 enhances female sexual female receptive sexualreceptive behavior through behavior a through specific a vomeronasal specific vomeronasal receptor. Nature receptor. 466, Nature 118-122 466, (2010) 118-122 (2010)3. Kim K, Sato K, Shibuya M, Zeiger DM, Butcher RA, Ragains JR, Clardy J, Touhara K.*Sengupta P. Two chemoreceptors mediate the the developmental effects of of dauer dauer pheromone inin C. C. elegans. Science 326, 326, 994-998 (2009)4. Touhara, K. and Vosshall, L.B. Sensing odorants and pheromones with chemosensoryreceptors. Annu. Rev. Physiol. 71, 307-332 (2009)5. Tanaka K, Uda Y, Y, Ono Ono Y, Nakagawa Y, Nakagawa T, Suwa T, Suwa M, Yamaoka M, Yamaoka R, *Touhara R, *Touhara K. Highly K. selective Highlyselective tuning of tuning a silkworm of a olfactory silkworm receptor olfactory to receptor a key mulberry to a key leaf mulberry volatile. leaf Current volatile. Biology Current 19,Biology 881-890 19, (2009) 881-890 (2009)6. Sato K, Pellegrino M, M, Nakagawa T, Nakagawa T, Nakagawa T, Vosshall T, Vosshall LB, *Touhara LB, *Touhara K. Insect K. olfactory Insectolfactory receptors receptors are heteromeric are heteromeric ligand-gated ligand-gated channels. channels. Nature 452, Nature 1002-1006 452, 1002-1006 (2008) (2008)7. Kimoto, H., Sato, K., K., Nodari, F., F., Haga, Haga, S., Holy, S., Holy, T., and T., *Touhara and *Touhara K. The K. mouse The ESP mouse family: ESPfamily: sex and sex strain and differences, strain differences, and implications and implications in the vomeronasal in the vomeronasal sensory system. sensory Current system.Current Biology 17, Biology 1879-1884 17, 1879-1884 (2007) (2007)8. Oka Y, Katada S, S, Omura M, M, Suwa M, M, Yoshihara Y, Y, *Touhara K. K. Odorant receptor receptor map map in the inthe mouse mouse olfactory bulb: bulb: in in vivo vivo sensitivity and and specificity of receptor-defined glomeruli.Neuron 52, 857-869 (2006)9. Kimoto H, Haga S, S, Sato Sato K, K, *Touhara K. K. Sex-specific peptides peptides released released from exocrine from exocrine glandsglands stimulate stimulate vomeronasal vomeronasal sensory sensory neurons neurons in mice. in mice.Nature 437, 898-901 (2005)10. Nakagawa T, Sakurai T, Nishioka T, *Touhara K. Insect sex-pheromone signals mediatedby specific combinations of olfactory receptors.Science 307, 1638-1642 (2005)6667

Invited SpeakersToward the circuit physiology of midbraindopamine Toward the circuit neurons: physiology beyond of midbrain stamp collectingdopamineneurons: beyond stamp collectingNaoshige UchidaHarvard UniversityNaoshige UchidaHarvard UniversityMidbrain dopamine neurons play pivotal roles in such brain functions as reward-basedlearning, motivation and movement. These neurons are located in the ventral tegmental area(VTA) and substantia nigra pars compacta (SNc). It has been postulated that dopamine neuronsbroadcast reward prediction error signals, i.e., the discrepancy between actual reward andexpected reward. While these observations have generated great interest, the underlyingmechanisms that regulate the firing patterns of dopamine neurons remain largely unknown.Recently, we have developed a mouse model to study neural circuits that regulate the activityof dopamine neurons. In a first experiment, mice are trained to associate different odors withdifferent outcomes (big reward, small reward, nothing and airpuff). We have recorded theactivity of VTA neurons while identifying their types optogenetically. In a second experiment,we have comprehensively identified monosynaptic inputs to midbrain dopamine neurons usingthe rabies virus-based transsynaptic, retrograde tracing. I will discuss these strategies forstudying neural circuits and implications into the mechanisms that regulate the activity ofdopamine neurons.Name: Naoshige UchidaAffiliation:Center for Brain ScienceDepartment of Molecular and Cellular BiologyHarvard UniversityBiography:Naoshige Uchida is an associate professor at the Center for Brain Science and Department ofMolecular and Cellular Biology at Harvard University, Massachusetts, USA. He did hisgraduate studies on molecular mechanisms of synaptic adhesions in Masatoshi Takeichi‘slaboratory at Kyoto University, Japan. He started studies on olfactory coding in Kensaku Mori‘slaboratory at the Brain Science Institute, RIKEN, Japan. He then joined Zachary Mainen‘slaboratory at Cold Spring Harbor Laboratory, New York, USA, where he startedpsychophysical experiments using rodent olfactory decision tasks. He studies neuralmechanisms of sensory coding, decision making, and reward-based learning and memory usingrodent psychophysics and multi-electrode recordings.Publications:Szuts, T., Fadeyev, V., Kachiguine, S., Sher, A., Grivich, M.V., Agrochao, M., Hottowy, P.,Dabrowski, W., Lubenov, E.V., Siapas, A.G., Uchida, N., Litke, A.M., Meister, M. (2011) Thebrain unplugged: A wireless multi-channel neural amplifier for freely moving animals. NatureNeurosci. 14: 263-269.Cury, K.M. and Uchida, N. (2010) Robust odor coding via inhalation-coupled transient activityin the mammalian olfactory bulb. Neuron, 68: 570-585.Kepecs, A., Uchida, N., Zariwala, H. and Mainen, Z. F. (2008) Neural correlates, computationand behavioural impact of decision confidence. Nature, 11;455(7210):227-31.Uchida, N. and Mainen, Z. F. (2008) Odor concentration invariance by chemical ratio coding.Front. Syst. Neurosci. 1:3. doi:10.3389/neuro.06/003.2007Kepecs, A., Uchida, N. and Mainen, Z. F. (2007) Rapid and precise control of sniffing duringolfactory discrimination in rats. J. Neurophysiol., 98: 205-213.Feierstein, C. E., Quirk, M. C., Uchida, N., Sosulski, D. L. and Mainen, Z. F. (2006)Representation of spatial goals in rat orbitofrontal cortex. Neuron, 51: 495-507.Gurden, H., Uchida, N. and Mainen, Z. F. (2006) Sensory-evoked intrinsic optical signals in theolfactory bulb are coupled to glutamate release and uptake. Neuron, 52: 335-45.Uchida, N., Kepecs, A., and Mainen, Z. F. (2006) Seeing at a glance, smelling in a whiff: rapidforms of perceptual decision-making. Nature Rev. Neurosci,. 7:485-491.Uchida, N., and Mainen, Z. F. (2003) Speed and accuracy of olfactory discrimination in the rat.Nature Neurosci. 6: 1224-1229.Uchida, N., Takahashi, Y.K., Tanifuji, M. and Mori, K. (2000) Odor maps in the mammalianolfactory bulb: domain organization and odorant structural features. Nature Neurosci. 3: 1035-1043.6869

Invited SpeakersGenes that are selectively expressed in regionsof primate Genes that neocortex: are selectively the expressed functions in regions ofand primate implication neocortex: for the cortical functions specializationand implication forcortical specializationTetsuo YamamoriNational Institute for Basic BiologyTetsuo YamamoriNational Institute for Basic BiologyThe neocortex, which is characteristic of mammals, has evolved to play important roles incognitive and perceptual functions. The localization of different functions in different regions ofthe neocortex was well established within the last century. Studies on the formation of theneocortex have advanced at the molecular level, thus successfully clarifying the mechanismsthat control neural or glial cell differentiation and sensory projections. However, mechanismsthat underlie cortical area specialization remain unsolved. To address this problem, our approachhas been to isolate and characterize the genes that are selectively expressed in particular subsetsof neocortical areas in primates; these areas are most distinctive among mammals. Bydifferential display and restriction landmark cDNA scanning (RLCS) methods, we haveidentified two major classes of genes that are specifically expressed in the adult macaquemonkey neocortical areas: One is expressed in the primary sensory areas, particularly, in theprimary visual cortex (V1) and the other is expressed in the association areas. The genes thatshow these specific expression patterns are limited to only several gene families among ourlarge-scale screening. The genes selectively expressed in primate V1 are serotonin receptors of5-HT1B and 5-HT2A and OCC1. In primate V1, 5-HT1B enhances the signal to noise (S/N)ratio and 5-HT2A works as a gain controller. Recently, Li et al, have shown that the product ofthe mouse homologue of OCC1 (fstl1) directly binds Na + , K + -ATPase and suppresses sensoryafferent synaptic transmission (Neuron, 69, 974-987, 2011). Therefore, the three genes that areselectively enriched in primate V1 control visual input-output relations so that the visualhomeostasis is retained under a dynamic range of visual inputs. The important feature in theseprimate V1 enriched genes is that their expressions are controlled in an activity-dependentmanner, some of which mechanisms may be different from those of rodents. The genesselectively expressed in primate association areas, are RBP, PNMA5, SAPRC and SLIT1.Although the role of these genes in primate association areas are largely unknown, we speculatethat they enhance dendritic branching and spine formation based on the morphological studiesin primates by Elston et al., (e.g., Proc. R.Soc. Lond. B., 266, 1367-1374, 1999) and molecularbiological studies of Slit1 in the rodent neocortex (Whitford et al., Annu. Rev. Neurosci., 25,127-149, 2009). Finally, I would like to talk our recent approaches toward proving thishypothesis using genetic manipulations in primates.Tetsuo YamamoriProfessor, National Institute for Basic Biology, Okazaki, Japan1980 March: Graduated from doctoral course (Biophysics) of Kyoto University, Japan1981 March: Dr. Sci. (Kyoto University)1981 October: Postdoctoral fellow, University of Colorado, Department of Molecular,Cellular and Developmental Biology, USA1986 March: Research fellow, California Institute of Technology, Biology Division,USA1991 March: Frontier Research Fellow, RIKEN, Japan1994 April to Present: Professor, National Institute for Basic Biology, Okazaki, JapanReferences1. Yamamori, T., Selective gene expression in regions of primate neocortex: implications forcortical specialization. Progress in Neurobiol., 94, 201-222, 2011.2. Takahata et al., Differential expression patterns of striate-cortex-enriched genes among OldWorld, New World, and prosimian primates. Cereb. Cortex (in press)2. Sasaki et al., Prefrontal-enriched SLIT1 expression in Old World monkey cortex establishedduring the postnatal development. Cereb. Cortex, 20, 2496-2510, 2010.3. Takaji et al., Paraneoplastic antigen-like 5 gene (PNMA5) is preferentially expressed in theassociation areas in a primate specific manner. Cereb. Cortex, 19:2865-2879, 2009.4. Takahata et al., Differential expression patterns of occ1-related genes in adult monkey visualcortex. Cereb. Cortex, 19: 1937-1951, 2009.5. Watakabe et al., Enriched expression of serotonin 1B and 2A receptor genes in macaquevisual cortex and their bidirectional modulatory effects on neuronal responses. Cereb. Cortex,19: 1915-1928, 2008.6. Takahata et al., Activity-dependent expression of occ1 in excitatory neurons is a characteristicfeature of the primate visual cortex. Cereb. Cortex, 16:929-940, 2006.7. Komatsu et al., Retinol-binding protein gene is highly expressed in higher-order associationareas of the primate neocortex. Cereb. Cortex, 15: 96-108, 2005.8. Tochitani et al., The OCC1 genes is preferentially expressed in the primary visual cortex in anactivity-dependent manner: a pattern of gene expression related to the cytoarchitectonic area insdult neocortex. Eur. J. Neurosci., 13, 297-307, 2001.7071

Invited SpeakersMolecular Genetic Dissectionof Olfactory Circuitry in Neural Zebrafish Circuitry in ZebrafishMolecular Genetic Dissection of Olfactory NeuralYoshihiro YoshiharaRIKEN Brain Science InstituteYoshihiro YoshiharaRIKEN Brain Science InstitutePositions and Employment:1989-1991 Postdoctoral Fellow, Department of Neuroscience, Osaka BioscienceInstitute1992-1996 Assistant Professor, Department of Biochemistry, Osaka Medical College1996-1998 Associate Professor, Department of Biochemistry, Osaka Medical College1998-2009 Team Leader, RIKEN Brain Science Institute2009-present Senior Team Leader, RIKEN Brain Science InstituteZebrafish has become one of the most useful model organisms in neurobiology. Inaddition to its general advantageous properties (external fertilization, rapid development,transparency of embryos, etc.), zebrafish is amenable to various genetic engineeringtechnologies such as transgenesis, mutagenesis, gene knockdown/knockout, andtransposon-mediated gene transfer. Our transgenic approach unraveled twosegregated neural pathways originating from ciliated and microvillous sensory neurons inthe olfactory epithelium to distinct regions of the olfactory bulb, which likely conveydifferent types of olfactory information (e.g. pheromones and odorants). Furthermore,the two basic principles (one neuron - one receptor rule and axon convergence to targetglomeruli) are essentially preserved also in zebrafish, rendering this organism a suitablemodel vertebrate for the olfactory research. In this talk, I will summarize recentadvances in our knowledge on the functional architecture of the olfactory neural circuitsin zebrafish, which mediate specific odor-induced behaviors. In particular, I will focuson molecular genetic dissection of the neural elements involved in the attraction to foododorants, the aversion from alarm pheromone, and the social response to sexpheromones.YOSHIHIRO YOSHIHARA, PH.D.Senior Team LeaderLaboratory for Neurobiology of SynapseRIKEN Brain Science InstituteRecent publicationsYoshihara Y. Molecular genetic dissection of the zebrafish olfactory system. InChemosensory Systems in Mammals, Fishes and Insects (eds. W. Meyerhof andS. Korsching) pp.97-120 (2009)Koide T, Miyasaka N, Morimoto K, Asakawa K, Urasaki A, Kawakami K, Yoshihara Y.Olfactory neural circuitry for attraction to amino acids revealed by transposon-mediatedgene trap approach in zebrafish. Proc. Natl. Acad. Sci. USA 106: 9884-9889 (2009)Miyasaka N, Morimoto K, Tsubokawa T, Higashijima S, Okamoto H, Yoshihara Y. From theolfactory bulb to higher brain centers: genetic visualization of secondary olfactorypathways in zebrafish. J. Neurosci. 29: 4756-4767 (2009)Kaneko-Goto T, Yoshihara S, Miyazaki H, Yoshihara Y. BIG-2 mediates olfactory axonconvergence to target glomeruli. Neuron 57: 834-846 (2008)Sato Y, Miyasaka N, Yoshihara Y. Hierarchical regulation of odorant receptor gene choiceand subsequent axonal projection of olfactory sensory neurons in zebrafish. J. Neurosci.27: 1606-1615 (2007)Miyasaka N, Knaut H, Yoshihara Y. Cxcl12/Cxcr4 chemokine signaling is required forplacode assembly and sensory axon pathfinding in the zebrafish olfactory system.Development 134: 2459-2468 (2007)Sato Y, Miyasaka N, Yoshihara Y. Mutually exclusive glomerular innervation by twodistinct types of olfactory sensory neurons revealed in transgenic zebrafish. J. Neurosci.25: 4889-4897 (2005)Miyasaka N, Sato Y, Yeo SY, Hutson LD, Chien CB, Okamoto H, Yoshihara Y. Robo2 isrequired for establishment of a precise glomerular map in the zebrafish olfactory system.Development 132: 1283-1293 (2005)Education:1980–1984 Faculty of Pharmaceutical Sciences, Kyoto University1984–1989 Department of Pharmacology, Graduate School of Pharmaceutical Sciences,Kyoto University: Ph.D., May 1989 Thesis Supervisor: Masamichi Satoh7273

Discussants

DiscussantsList of publicationKohei HattaKohei HattaUniveristy of HyogoKohei HattaUniveristy of HyogoMoly P.K., Hatta, K. Early glycinergic axon contact with the Mauthner neuron during zebrafishdevelopment. Neurosci. Res. 70:251-9 (2011)Ikenaga T, Urban JM, Gebhart N, Hatta K, Kawakami K, Ono F. Formation of the spinal network in zebrafishdetermined by domain-specific pax genes. J Comp Neurol 519:1562-79 (2011)Personal DataName:Address:Kohei HattaGraduate School of Life Science Univeristy of Hyogo3-2-1 Kouto, Kamigori, Ako-gun, Hyogo 678-1297, JapanHashimoto M, Shinohara K, Wang J, Ikeuchi S, Yoshiba S, Meno C, Nonaka S, Takada S, Hatta K,Wynshaw-Boris A, Hamada H. Planar polarization of node cells determines the rotational axis of nodecilia. Nature Cell Biology 12:170-6 (2010)Deguchi, T., Itoh, M., Urawa, H., Matsumoto, T., Nakayama, S., Kawasaki, T., Kitano, T., Oda, S., Mitani, H.,Takahashi, T., Toda, T., Sato, J., Okada, K. , Hatta, K. *(corresponding authorfor the work with zebrafish),Yuba, S. and Kamei Y. Infrared laser-mediated local gene induction in medaka, zebrafish andArabidopsis thaliana. Dev. Growth Differ. 51:769-775 (2009)Kurotaki, Y., Hatta, K. *(corresponding author for the photoconvertible mice), Nakao, K., Nabeshima, Y. &Fujimori, T. Blastocyst axis is specified independently of early cell lineage but aligns with the ZP shape.Science 316, 719-23 (2007)Education1988 Ph. D. Graduate School of Life Science, University of Kyoto, Japan1983 B. Sc. Department of Biology, University of Kyoto, JapanAcademic positions and employment2007~ : Professor, Graduate School of Life Science, University of Hyogo, Japan2002~ : Research Associate, Center for Developmental Biology, Riken, Japan1996~ : Postdoctral Fellow, Institut Pasteur, Laboratoire de NeurobiologieCellulaire et Moleculaire, France1983~ : Postdoctral Fellow, Univerisity of Oregon, Institute of Neuroscience, USAHatta, K., Tsujii, H. and Omura, T.Protocols 1: 960 - 967 (2006)Cell tracking using a photoconvertible fluorescent protein. NatureHatta, K., Ankri, N., Faber, D.S., and Korn, H. Slow inhibitory potentials in the teleost Mauthner cell.Neuroscience. 103(2):561-579 (2001)Hatta, K. and Korn, H. Tonic inhibition alternates in paired neurons that set direction of fish escape reaction.Proc. Natl. Acad. Sci. USA. 96:12090-12095 (1999)Hatta, K., Püschel, A.W., and Kimmel, C.B. Midline signaling in the primordium of the zebrafish anteriorcentral nervous system. Proc. Natl. Acad. Sci. USA. 91:2061-2065 (1994)Hatta, K. Role of the floor plate in axonal patterning in the zebrafish CNS. Neuron 9:629-642 (1992)Hatta, K., Kimmel, C.B., Ho, R.K., and Walker, C. (1991) The cyclops mutation blocks specification of thefloor plate of the zebrafish central nervous system. Nature 350:339-341Hatta, K., Schilling, T.F., BreMiller, R.A., and Kimmel, C.B. (1990) Specification of jaw muscle identity inzebrafish: correlation with engrailed-homeoprotein expression. Science 250:802-805Kimmel, C.B., Hatta, K., and Metcalfe, W.K. (1990) Early axonal contacts during development of anidentified dendrite in the brain of the zebrafish. Neuron 4:535-545Miyatani S, Shimamura K, Hatta M, Nagafuchi A, Nose A, Matsunaga M, Hatta K, and Takeichi M. (1989)Neural cadherin: role in selective cell-cell adhesion. Science 245(4918):631-5.Matsunaga M, Hatta K, Nagafuchi A, Takeichi M. (1988) Guidance of optic nerve fibres by N-cadherinadhesion molecules. Nature 334:62-4.Matsunaga M, Hatta K, Takeichi M. (1988) Role of N-cadherin cell adhesion molecules in thehistogenesis of neural retina. Neuron 1:289-95.Hatta K, Nose A, Nagafuchi A, Takeichi M. (1988) Cloning and expression of cDNA encoding a neuralcalcium-dependent cell adhesion molecule: its identity in the cadherin gene family. J Cell Biol. 106:873-81.Hatta K, Takeichi M. (1986) Expression of N-cadherin adhesion molecules associated with earlymorphogenetic events in chick development.Nature 320:447-9.Hatta K, Okada TS, Takeichi M. (1985) A monoclonal antibody disrupting calcium-dependent cell-celladhesion of brain tissues: possible role of its target antigen in animal pattern formation. Proc Natl Acad SciU S A. 82:2789-93.7677

Awards and ScholarshipHiruma-Wagner Award, Research Foundation for Opto-Science andTechnology, 2010DiscussantsYoung Investigator Award of Japan Neuroscience Society, 2009.Yukiyasu Kamitani, Ph.D.Research andWork ExperienceYukiyasu KamitaniATR Computational Neuroscience LaboratoriesDepartment of NeuroinformaticsATR Computational Neuroscience Laboratories2-2-2 Hikaridai, Keihanna Science CityKyoto 619-0288, JapanPhone: +81-774-95-1212Fax: +81-90-2047-7123Email: kmtn@atr.jpHead of Department of Neuroinformatics, 2008-PresentATR Computational Neuroscience Laboratories, Kyoto, Japan.Professor, 2010-PresentNara Institute of Science and Technology, Nara, Japan.Senior Research Scientist, 2007-2008ATR Computational Neuroscience Laboratories, Kyoto, Japan.Associate Professor, 2006-2010Nara Institute of Science and Technology, Nara, Japan.Researcher, 2004-2007ATR Computational Neuroscience Laboratories, Kyoto, Japan.Visiting Research Stuff, 2003-2004Princeton University, Princeton, MA, USA.Research Fellow (SPD), 2003-PresentUniversity of Tokyo, and the Japan Society for the Promotion of Science,Tokyo, Japan.Research Fellow, 2001-2003Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA,USA.Selected PublicationsAsahi 21 Square Award, 2009Paper Award of Japanese Neural Network Society, 2009Research Award of Japanese Neural Network Society, 2006Scientific American 50 (named “Research Reader in Neural Imaging”), 2005Postdoctoral Fellowship of the Japan Society for the Promotion of Science forYoung Scientists (SPD), 2003-2006Uehara Memorial Foundation Postdoctoral Fellowship, 2001-2002Research Fellowship of the Japan Society for the Promotion of Science forYoung Scientists (DC), 1996-1998Scholarship of the Japan Scholarship Foundation, 1993-1994Yanagisawa, T., Hirata, M., Saitoh, Y., Kishima, H., Matsushita, K., Goto, T.,Fukuma, R., Yokoi, H., Kamitani, Y., and Yoshimine, T. (2011 in press).Electrocorticographic control of a prosthetic arm in paralyzed patients. AnnNeurolToda, H., Suzuki, T., Sawahata, H., Majima, K., Kamitani, Y., and Hasegawa,I. (2011). Simultaneous recording of ECoG and intracortical neuronal activityusing a flexible multichannel electrode-mesh in visual cortex. Neuroimage 54,203-212.Kamitani, Y., and Sawahata, Y. (2010). Spatial smoothing hurts localizationbut not information: Pitfalls for brain mappers. Neuroimage 49, 1949-1952.Yamashita, O., Sato, M., Yoshioka, T., Tong, F., and Kamitani, Y. (2008).Sparse estimation automatically selects voxels relevant for the decoding offMRI activity patterns. Neuroimage 42, 1414-1429.Miyawaki, Y., Uchida, H., Yamashita, O., Sato, M. A., Morito, Y., Tanabe, H.C., Sadato, N., and Kamitani, Y. (2008). Visual image reconstruction fromhuman brain activity using a combination of multiscale local image decoders.Neuron 60, 915-929.Kamitani, Y. and Tong, F. (2006). Decoding seen and attended motiondirections from activity in the human visual cortex. Curr Biol 16, 1096-1102.EducationPh.D. in Computation and Neural Systems, 2001California Institute of Technology, Pasadena, CA.M.S. in Philosophy of Science, 1995University of Tokyo, Tokyo, Japan.B.A. in Cognitive and Behavioral Sciences, 1993University of Tokyo, Tokyo, Japan.Kamitani, Y. and Tong, F. (2005). Decoding the visual and subjectivecontents of the human brain. Nat Neurosci 8, 679-685.Shimojo, S., Kamitani, Y., and Nishida, S. (2001). Afterimage of perceptuallyfilled-in surface. Science 293, 1677-1680.Kamitani, Y., Bhalodia, V. M., Kubota, Y., and Shimojo, Y. (2001). A model ofmagnetic stimulation of neocortical neurons. Neurocomput. 38-40, 697-703.Shams, L., Kamitani, Y., and Shimojo, S. (2000). Illusions. What you see iswhat you hear. Nature 408, 788.Awards and ScholarshipHiruma-Wagner Award, Research Foundation for Opto-Science andTechnology, 2010Kamitani, Y. and Shimojo, S. (1999). Manifestation of scotomas created bytranscranial magnetic stimulation of human visual cortex. Nat Neurosci 2,767-771.Young Investigator Award of Japan Neuroscience Society, 2009.Asahi 21 Square Award, 20097879

Noriko OsumiTohoku University School of MedicineOsumi Publication List (short ver)DiscussantsNoriko OsumiTohoku University School of Medicine13) Hara, Y., et al.: Impaired hippocampal neurogenesis and vascular formation inephrin-A5-deficient mice. Stem Cells. 28(5), 974-983, 2010.14) Maekawa, M., et al.: Giant Subependymoma Developed in a Patient with Aniridia:Analyses of PAX6 and Tumor-relevant Genes. Brain Pathol. 20(6), 1033-1041, 2010.15) Umeda, T., et al.: Evaluation of Pax6 mutant rat as a model for autism. PloS One. 5(12),e15500, 2010.16) Takahashi, M. and Osumi, N.: Pax6 regulates boundary-cell specification in the rathindbrain. Mech. Dev. 128(5-6), 289-302, 2011.Selected Research Articles:1) Matsuo, T. *, Osumi-Yamashita, N. *, et al.: A mutation in the Pax-6 gene in rat small eyeis associated with migration defect of midbrain crest cells. Nat Genet. 3(4), 299-304, 1993.(*equally contributed)2) Osumi-Yamashita, N., et al.: The contribution of both forebrain and midbrain crest cells tothe mesenchyme in the frontonasal mass of mouse embryos. Dev Biol. 164(2), 409-419,1994.3) Osumi, N., et al.: Pax-6 is involved in specification of the hindbrain motor neuron subtype.Development. 124(15), 2961-2972, 1997.4) Akamatsu, W., et al.: Mammalian ELAV-like neuronal RNA-binding proteins HuB andHuC promote neuronal development in both the central and the peripheral nervous systems.Proc Natl Acad Sci U S A. 96(17), 9885-9890, 1999.5) Inoue, T., et al.: Role of cadherins in maintaining the compartment boundary between thecortex and striatum during development. Development. 128(4), 561-569, 2001.6) Takahashi, M. and Osumi, N.: Pax6 regulates specification of ventral neuron subtypes inthe hindbrain by establishing progenitor domains. Development. 129(6), 1327-1338, 2002.7) Nomura, T. and Osumi, N.: Misrouting of mitral cell progenitors in the Pax6/Small eye rattelencephalon. Development. 131(4), 787-796, 2004.8) Tomita, Y., et al.: Cardiac neural crest cells contribute to dormant multipotent stem cells inthe mammalian heart. J Cell Biol. 170(7), 1135-1146, 2005.9) Watanabe, A., et al.: Fabp7 maps to a quantitative trait locus for a schizophreniaendophenotype. PLoS Biol. 5(11), e297, 2007.10) Sakurai, K. and Osumi, N.: The neurogenesis-controlling factor, Pax6, inhibitsproliferation and promotes maturation in murine astrocytes. J Neurosci. 28(18), 4604-4612,2008.11) Maekawa, M., et al.: Arachidonic acid drives postnatal neurogenesis and elicits abeneficial effect on prepulse inhibition, a biological trait of psychiatric illnesses. PLoS ONE.4(4), e5085, 2009.12) Maekawa, M., et al.: A novel missense mutation (Leu46Val) of PAX6 found in an autisticpatient. Neurosci Lett. 462(3), 267-271, 2009.8081

Curriculum Vitae2006 NISTEP Award from MEXTName: Noriko, OSUMI, DDS, PhDPresent position: ProfessorDepartment of Developmental NeuroscienceCenter for Translational and Advanced Animal ResearchTohoku University School of MedicineAddress: 2-1, Seiryo-machi, Aoba-ku, Sendai 980-8575, JapanTel: -81-22-717-8201FAX: -81-22-717-8205E-mail: osumi@mail.tains.tohoku.ac.jpAcademic and Professional Career1979-1985 School of Dentistry, Tokyo Medical & Dental University1985-1989 Graduate School of Dentistry, Tokyo Medical & Dental University1989-1996 Research Associate, Dep artment of Craniofacial Morphogenes isand Anomalies, Tokyo Medical & Dental University1996-1998 Associate Professor, National Institute of Neuroscience, NationalCenter of Neurology & Psychiatry1998- Present position2007- Special Advisor for Gender Equality (Tohoku University)2008-2010 Distinguished Professor (Tohoku University)Award1985 Nagao Award from S chool of D entistry, Tokyo Medical & Dent alUniversity (for the top student on graduation)1992 Hatton Travel Award from In ternational Association for Dent alResearch for the 70th General Session of the IADRCommittees (only selected):Organizing member, Japanese Society of Developmental BiologistsOrganizing member, Japanese Society for Cell BiologyOrganizing member, Japanese Neuroscience SocietyEditorial Board, Development Growth & DifferentiationEditorial Board, Genes to CellsEditorial Board, J AnatomyMember, Peer Review Committee for Governmental Grants (MEXT)Member, Advisory Committee for Life Science (MEXT)Member, Committee for Ethical Problems in Human ES CellsProgram Officer, Special Grants for Priority Research (JST)Member, Committee for National Institute of GeneticsMember, Science Council of JapanBiosketchProf. Osumi has graduated Tokyo Medical and Dental University, been given PhDthesis from the same university, and now is a professor of Tohoku University Schoolof Medicine since 1998. She has recently been chosen as one of 25 DistinguishedProfessors in Tohoku University. She is appointed in various governmentalcommittees such as ethical issues, grant system development, and career paths foryoung scientists, and also chosen as a youngest member of Japanese CouncilJapan since 2005. Her research interest covers broad areas such as pre- andpostnatal development of the brain and craniofacial region, and behavior of animalsas models of psychiatric diseases. More specifically, she is recently eager tounderstand regulatory mechanisms of neurogenesis and maintenance of neuralstem cells at cellular and molecular levels both in embryonic and postnatal stages.Manipulating embryos and imaging brain cells are expertise of her lab. She hastranslated two books into Japanese: Essential Developmental Biology by JonathanSlack and The Birth of the Mind by Gary Marcus. She is a representative of CRESTproject (2005-2010) supported by JST and Global COE project (2007-2012)supported by MEXT.82 83

Takeshi SakuraiKyoto UniversityDiscussantsTakeshi Sakurai, M.D., Ph.D.Takeshi SakuraiKyoto UniversityEDUCATION, RESEARCH, AND PROFESSIONAL EXPERIENCE1988 M.D., Nagoya University School of Medicine, Nagoya, Japan1988-1989 Internship (Resident of Internal Medicine), St. Luke's International Hospital,Tokyo, Japan1993 Ph.D., Nagoya University Graduate School of Medicine, Nagoya, Japan1993-1997 Postdoctoral Associate, New York University Medical Center, New York, Dept.Pharmacology1997-1999 Research Associate, New York University Medical Center, New York, Dept.Pharmacology2000-2001 Research Assistant Professor, Rutgers, State University of New Jersey,Piscataway, New Jersey, Keck Center for Collaborative Neuroscience2001-2002 Research Assistant Professor, Mount Sinai School of Medicine, New York, NewYork, Dept. Neurology and Neuroscience2002-2011 Assistant Professor, Mount Sinai School of Medicine, New York, New YorkDept. Psychiatry and Pharmacology and Systems Therapeutics and Neurology2011-present Associate Professor, Kyoto University Graduate School of Medicine, Kyoto,Kyoto, Japan, Medical Innovation CenterPUBLICATIONS (selected from total 53 originals, reviews, and book chapter)1 Elior Peles, Moshe Nativ, Phillip L. Campbell, Takeshi Sakurai, Ricardo Martinez, Sima Lev,Douglas O. Clary, James Schilling, Gilad Barnea, Gregory D. Plowman, Martin Grumet and JosephSchlessinger. The carbonic anhydrase domain of receptor tyrosine phosphatase is a functionalligand for the axonal cell recognition molecule contactin. Cell, 82, 251-260, 1995.2 Takeshi Sakurai, Marc Lustig, Moshe Nativ, John J. Hemperly, Joseph Schlessinger, Elior Peles andMartin Grumet. Induction of neurite outgrowth through contactin and Nr-CAM by extracellularregions of glial receptor tyrosine phosphatase . Journal of Cell Biology, 136, 907-918, 19973 Marc Lustig, Lynda Erskine, Carol A. Mason, Martin Grumet, and Takeshi Sakurai. Nr-CAMexpression in the developing mouse nervous system: Ventral midline structures, specific fiber tracts,and neuropilar regions. Journal of Comparative Neurology, 434, 13-28, 20014 Takeshi Sakurai, Marc Lustig, Joanne Babiarz, Andrew J.W. Furley, Steven Tait, Peter J. Brophy.Stephen A. Brown, Lucia Y. Brown, Carol A. Mason and Martin Grumet. Overlapping functions ofthe cell adhesion molecules Nr-CAM and L1 in cerebellar granule cell development. Journal of CellBiology, 154, 1259-1273, 20015 Scott E. Williams, Fanny Mann, Lynda Erskine, Takeshi Sakurai, Shiniu Wei, Derrick J. Rossi,Nicholas W. Gale, Christine E. Holt, Carol A. Mason and Mark Henkemeyer. Ephrin-B2 and EphB1mediate retinal axon divergence at the optic chiasm. Neuron, 39, 919-935, 20036 Scott E. Williams, Martin Grumet, David R. Colman, Mark Henkemeyer, Carol A. Mason, andTakeshi Sakurai. A role for Nr-CAM in the patterning of binocular visual pathways. Neuron, 50,535-547, 20067 Shin Yasuda, Hidekazu Tanaka, Hiroko Sugiura, Ko Okamura, Taiki Sakaguchi, Uyen Tran, TakakoTakemiya, Akira Mizoguchi, Yoshiki Yagita, Takeshi Sakurai, Edward M. De Robertis, and KanatoYamagata. Activity-induced protocadherin arcadlin regulates dendritic spine number by triggeringN-cadherin endocytosis via TAO2 and p38 MAP kinases. Neuron, 56, 456-471, 20078 Joseph D. Buxbaum, Lyudmila Georgieva, James J. Young, Christopher Plescia, Yuji Kajiwara, YuhuiJiang, Valentina Moskvina, Nadine Norton, Tim Peirce, Hywel J. Williams, Nick J. Craddock, LiamCarroll, Gabriel Corfas, Kenneth L. Davis, Michael Owen, Sheila Harroch, Takeshi Sakurai, andMichael C. O’Donovan. Molecular dissection of NRG1-ERBB4 signaling implicates PTPRZ1 as apotential schizophrenia susceptibility gene. Molecular Psychiatry, 13, 162-172, 20089 Kai Wang, Haitao Zhang, Deqiong Ma, Maja Bucan, Joseph T. Glessner, Brett S. Abrahams, DariaSalyakina, Marcin Imielinski, Jonathan P. Bradfield, Patrick M.A. Sleiman, Cecilia E. Kim, CuipingHou, Edward Frackelton, Rosetta Chiavacci, Nagahide Takahashi, Takeshi Sakurai, Eric Rappaport,Clara M. Lajonchere, Jeffrey Munson, Annette Estes, Olena Korvatska, Joseph Piven, Lisa I.Sonnenblick, Ana I. Alvarez Retuerto, Edward I. Herman, Hongmei Dong, Ted Hutman, MarianSigman, Sally Ozonoff, Ami Klin, Thomas Owley, John A. Sweeney, Camille W. Brune, Rita M.Cantor, Raphael Bernier, John R. Gilbert, Michael L. Cuccaro, William M. McMahon, Judith Miller,Matthew W. State, Thomas H. Wassink, Hilary Coon, Susan E. Levy, Robert T. Schultz, John I.Nurnberger Jr., Jonathan L. Haines, James S. Sutcliffe, Edwin H. Cook Jr., Nancy J. Minshew, JosephD. Buxbaum, Geraldine Dawson, Struan F.A. Grant, Daniel H. Geschwind, Margaret A. Pericak-Vance, Gerard D. Schellenberg, and Hakon Hakonarson. Common genetic variants on 5p14.1associate with autism spectrum disorders. Nature, 459, 528-533, 200910 Joseph T. Glessner, Kai Wang, Guiqing Cai, Olena Korvatska, Cecilia E. Kim, Shawn Wood, HaitaoZhang, Annette Estes, Camille W. Brune, Jonathan P. Bradfield, Marcin Imielinski, Edward C.Frackelton, Jennifer Reichert, Emily L. Crawford, Jeffrey Munson, Patrick M.A. Sleiman, RosettaChiavacci, Kiran Annaiah, Kelly Thomas, Cuiping Hou, Wendy Glaberson, James Flory, FrederickOtieno, Maria Garris, Latha Soorya, Lambertus Klei, Joseph Piven, Kacie J. Meyer, EvdokiaAnagnostou, Takeshi Sakurai, Rachel M. Game, Danielle S. Rudd, Danielle Zurawiecki,Christopher J. McDougle, Lea K. Davis, Judith Miller, David J. Posey, Shana Michaels, AlexanderKolevzon, Jeremy M. Silverman, Raphael Bernier, Susan E. Levy, Robert T. Schultz, GeraldineDawson, Thomas Owley, William M. McMahon, Thomas H. Wassink, John A. Sweeney, John I.Nurnberger Jr., Hilary Coon, James S. Sutcliffe, Nancy J. Minshew, Struan F.A. Grant, Maja Bucan,Edwin H. Cook Jr., Joseph D. Buxbaum, Bernie Devlin, Gerard Schellenberg, and Hakon Hakonarson.Autism genome-wide copy number variation reveals ubiquitin and neuronal genes. Nature, 459, 569-573, 200911 Catalina Betancur, Takeshi Sakurai, and Joseph D. Buxbaum. The emerging role of synaptic celladhesionpathways in the pathogenesis of autism spectrum disorders. Trends in Neurosciences, 32,402-412, 200912 Takeshi Sakurai, Nicolas Romoz, Marta Barreto, Mihaela Gazdoiu, Nagahide Takahashi, MichaelGertner, Nathan Dorr, Miguel A. Gama Sosa, Rita De Gasperi, Gissel Perez, James Schmeidler,Vivian Mitropoulou, H. Carl Le, Mihaela Lupu, Patrick R. Hof, Gregory A. Elder, and Joseph D.Buxbaum. Slc25a12 disruption alters myelination and neurofilaments: a model for a hypomyelinationsyndrome and childhood neurodevelopmental disorders. Biological Psychiatry, 67, 887-894, 201013 Nagahide Takahashi, Takeshi Sakurai, Kenneth Davis, and Joseph D. Buxbaum. Linkingoligodendrocyte and myelin dysfunction to neurocircuitry abnormalities in schizophrenia. Progress inNeurobiology, 93, 13-22, 201014 Takeshi Sakurai, Guiqing Cai, Dorothy E. Grice, and Joseph D. Buxbaum. The genomic architectureof autism spectrum disorders. Chapter in Textbook of Autism spectrum disorders. Eric Hollander,Alexander Kolevzon, Joseph Coyle, editors. American Psychiatric Publishing Inc., 281-298, 201015 Dia Xenaki, Indira Martin, Lynn Yoshida, Kyoji Ohyama, Gianfranco Gennarini, Martin Grumet,Takeshi Sakurai and Andrew J.W. Furley. F3/contactin and TAG1 play antagonistic roles in theregulation of sonic hedgehog-induced cerebellar granule neuron progenitor proliferation.Development, 138, 519-529, 201116 Galina P. Demyanenko, Thorfinn T. Riday, Tracy S. Tran, Jasbir Dalal, Eli P. Darnell, Leann H.Brennaman, Takeshi Sakurai, Martin Grumet, Benjamin D. Philpot, and Patricia F. Maness.NrCAM deletion causes topographic mistargeting of thalamocortical axons to the visual cortex anddisrupts visual acuity. Journal of Neuroscience, 31, 1545-1558, 201117 Takeshi Sakurai, Nathan P. Dorr, Nagahide Takahashi, L. Alison McInnes, Gregory A. Elder, andJoseph Buxbaum. Haploinsufficiency of Gtf2i, a gene deleted in Williams syndrome, leads toincrease in social interactions. Autism Research, 4, 28-39, 201118 Nagahide Takahashi, Takeshi Sakurai, Ozlem Bozdagi-Gunal, Nathan P. Dorr, Joanne Moy, LisaKrug, Miguel Gama-Sosa, Gregory A. Elder, Rick J. Koch, Ruth H. Walker, Patrick, R. Hof, KennethL. Davis, and Joseph D. Buxbaum. Increased expression of receptor phosphotyrosine phosphatase-/, is associated with molecular, cellular, behavioral and cognitive schizophrenic phenotypes.Translational Psychiatry, 1, e8, 1-10, 20118485

Poster Presenters

Poster PresentersNeural mechanisms for stereoscopic depth perceptionNeural mechanisms for stereoscopic depthperception in macaque V4:Responses to graded anti-correlationin macaque V4: Responses to graded anti-correlationMohammad AbdolrahmaniGraduate School of Frontier Biosciences, Osaka UniversityMohammad AbdolrahmaniGraduate School of Frontier Biosciences, Osaka UniversityAbstractHumans perceive the three dimensional world by solving the stereocorrespondence problem, which refers to the problem of matching the visualfeatures in one eye’s image to those in the other eye’s image. Perception ofstereoscopic depth diminishes when the solution for the correspondenceproblem does not exist. This happens for anti-correlated random-dotstereograms (aRDS), in which all elements of one eye’s image is contrastreversed with respect to those of the other eye's image. The ventral visualpathway implements the neural solution for the correspondence problem. Thefalse information about the depth (i.e., inverted disparity energy values) of aRDSis first encoded in the primary visual cortex but later discarded gradually by amid-level area, V4, and a higher-level area, inferior temporal cortex.To better understand the neural implementation of the stereo correspondencesolution, we examined responses of V4 neurons to graded anti-correlation ofRDSs by decreasing the percentage of binocularly contrast-matched dots (matchlevel) gradually. By performing single-unit recordings from area V4 in a macaqueusing this set of stimuli, we investigated a further correlation between theneuronal and perceptual performances.We found that the neuronal disparity selectivity decreased sharply as thebinocular match level decreased from 100% to 50%, but did not decrease largelyfor the match levels from 50% to 0%. This neuronal behavior is in sharp contrastto human stereo perception: a recent psychophysical study shows that (fine)depth perception is intact down to 50% match level but deteriorates for thematch levels from 50% to 0% (Doi et al., 2011, J Vision).Our preliminary results suggest that the neural responses in V4 are notconsistent with stereoscopic depth if we consider responses not only at zero andfull anti-correlation but also at graded levels of anti-correlation.References:Takahiro Doi, Seiji Tanabe, and Ichiro Fujita, Matching and correlation computations instereoscopic depth perception, J Vis March 2, 2011 11(3): 1Curriculum VitaMohammad AbdolrahmaniPhD student, Laboratory for Cognitive Neuroscience (Fujita lab), Scholl of frontierBiosciences (FBS), Osaka UniversityCourses1. Research student at Laboratory for cognitive Neuroscience, FBS, OsakaUniversity, May-October 20092. Osaka University Global COE and IBRO-APRC Summer School of Neuroscience2008, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan3. Australian National University, research school of biological sciences, SummerSchool of Neuro-ethology, Feb 2009, Canberra, AustraliaInternational Conferences1. Abdolrahmani M., Jameie SB. The effects of light deprivation on posterior parietalcortex in rats. Australian Neuroscience Society Conference, Jan 2009, Canberra2. Abdolrahmani M., Jameie SB., Nobakht M., Effects of light deprivation on lateralgeniculate nucleus in rat neonates, Fifth Asian Pacific International Congress ofAnatomy, Tehran, Iran, 20083. Jameie SB., Abdolrahmani M., Nobakht M., Roozdar B., Tabatabaei P., Retinalmechanisms induce synaptic plasticity in SCN and dLGN in light deprived ratneonates: Electron and light microscopic studies, Fifth Asian Pacific InternationalCongress of Anatomy, Iran, 20084. Jameie SB., Abdolrahmani M., Nobakht M., Roozdar B., Tabatabaei P., Retinalmechanisms induce synaptic plasticity in SCN and dLGN in light deprived ratneonates: Electron and light microscopic studies, European Retina Meeting,Frankfort, Germany, 2007Publications:1. Seyed Behnam E-Din Jameie, Mohammad Abdolrahmani, Maliheh Nobakht.Effects of Total Light Deprivation on Dorsal Lateral Geniculate Nucleus of MaleNeonate Rats, Oman medical journal, 2010. 53, p: 179-1832. Abdolrahmani M., Jameie SB. Gradual increases in neuronal density of rats'LGN from anterior to posterior. Neurosciences Journal, 2009. 14(2), p: 7-108889

Poster PresentersDirect comparison between humans and chimpanzees for theirDirect comparison between humans andchimpanzees for their pitch-liminance mappingpitch-liminance mappingIkuma AdachiKyoto UniversityAbstract:Ikuma AdachiKyoto UniversityIn synaesthesia, input to one sensory modality leads to automatic and vivid secondary experiences.For example, sound-colour synaesthetes see colours when they hear sounds. All humans experiencesuch (or similar) cross-modal correspondences to some extent, which has been termed weaksynaesthesia. Most prominently, already human toddlers associate high pitch sounds with lightercolours than low pitch sounds, and sound-colour synaesthetes map in this same direction. It has beenargued that the tendency to systematically match visual and auditory dimensions was a driving factorin the evolution of language, which might also explain the evolution of synaesthesia. However, nonehas yet addressed the crucial issue if non-human animals experience cross-modal correspondences aswell. Here we provide the first direct comparison between humans and chimpanzees on theirpitch-luminance mapping. Participants from both species were required to classify squares as blackor white, while hearing irrelevant background sounds that were either high-pitched or low-pitched.Chimpanzees made more mistakes when the background sound was synaesthetically incongruent(low-pitched for white, high-pitched for black) than when it was synaesthetically congruent(high-pitched for white, low-pitched for black). In humans, the effect was evident through increasedlatencies in incongruent trials in line with previous research. These results suggest that suchcross-modal correspondence are shared in these two species tested here and synaesthesia andcross-modal associations in non-synaesthetes partly reflect evolutionary old mechanisms in theprimate brain.Ikuma Adachi Ph.D.Center for International Collaborations and Advanced Studies in Primatology(CICASP)Primate Research Institute, Kyoto UniversityKanrin, Inuyama-city, Aichi, 484-8506, Japane-mail; adachi@pri.kyoto-u.ac.jpEDUCATION AND TRAINING2010(Apr)-:Assistant Professor: Center for International Collaboration and Advanced Studies in Primatology, PrimateResearch Institute, Kyoto University, Aichi, Japan.2009(Jan)-:Program-Specific Assistant Professor: Primate Research Institute, Kyoto University, Aichi, Japan.2008(Apr)-2008(Dec): Postdoc fellow: Primate Research Institute, Kyoto University, Aichi, Japan.2006(Apr)-2008(Mar): Postdoc fellow: Yerkes Primate Research Center, Emory University, GA, USA.2006(Mar): Ph.D. Psychology, Graduate School of Letters, Kyoto University, Kyoto, Japan2003(Mar): M. A. Psychology, Graduate School of Letters, Kyoto University, Kyoto, Japan2001(Mar): B. S. Psychology, Faculty of Letters, Kyoto University, Kyoto, JapanSELECTED RECENT PUBLICATONS (PEER REVIEWED PAPERS)1. Ludwig V.*, Adachi, I.*, Matsuzawa, T. (under revision). Can you see sounds? Chimpanzees associate highauditory pitch with visual lightness. Proceedings of the National Academy of Sciences* These authors contributed equally to this work.2. Adachi, I., Hampton, RR. (2011). Rhesus monkeys see who they hear: Spontaneous cross-modal memory forfamiliar conspecifics. PLoSONE, 6(8): e23345. doi:10.1371/journal.pone.0023345.3. Adachi, I., Anderson, JR., Fujita, K. (2011). Reverse-Reward Learning in squirrel monkeys (Saimiri sciureus):Five-Year Assessment, and Tests for Qualitative Transfer. Journal of Comparative Psychology, 125, pp. 84-90.4. Paxton, R., Basile, BM., Adachi, I., Suzuki, WA., Wilson, ME., Hampton, RR. (2010) Rhesus monkeys(Macaca mulatta) rapidly learn to select dominant individuals in videos of artificial social interactions betweenunfamiliar conspecifics. Journal of Comparative Psychology, 124, pp. 395-401.5. Adachi, I., Chou, DP., Hampton, RR. (2009)Thatcher effect in monkeys demonstrates conservation of face perception across primates. Current Biology,Volume 19, Issue 15, pp. 1270-1273.6. Adachi, I. (2009). Cross-modal representations in primates and dogs: A new framework of recognition of socialobjects. Intraction Studies, Volume 10, Issue 2, pp. 225-251.7. Adachi, I., Kuwahata H., Fujita, K., Tomonaga M., Matsuzawa T. (2009). Plasticity of ability to formcross-modal representations in infant Japanese macaques. Developmental Science, Volume 12, Issue 3,pp.446-452.8. Adachi, I. Fujita, K. (2007). Cross-modal representation of human caretakers in squirrel monkeys. BehaviouralProcesses, Volume 74, Issue 1, pp. 27-32.9. Adachi, I., Kuwahata, H., Fujita, K. (2007). Dogs recall owner's face upon hearing owner's voice. AnimalCognition, Volume 10, Issue 1, pp. 17-21.9091

Poster PresentersTitle of poster presentation Monoallelic genesin single olfactory neuronsTitle of poster presentation Monoallelic genes in singleolfactory neuronsMing-Shan ChienDuke UniversityAbstractMing-Shan ChienDuke UniversityThough typical autosomal genes are thought to be transcribed from both alleles,recent evidence suggests that many genes may be only active on one allele,either by imprinting or random monoallelic choice. Identification of suchmonoallelic genes is fundamental to understand not only how epigeneticregulation works in each gene but also the possible mechanisms of diseaseswith dominant or semi dominant traits. In neurons, however, it was challenging tostudy genes that show random monoallelic expression or imprinting in only asubset of neurons, because of the inability to expand the clonal population ofmature neurons and the immense heterogeneity of neurons. Here we use singlemouse olfactory sensory neurons as a model to analyze genome-wide allelicexpression.We amplified cDNA from single dissociated olfactory neurons derived from F1of C57BL/6J and SPRET/EiJ. We sequenced seven samples by Illuminasingle-end sequencing for 36 bases per read. The reads were aligned to bothC57BL/6J and SPRET/EiJ genome sequence by bowtie short read aligner thatallows 1-2 mismatches per read. The single nucleotide polymorphisms (SNPs)were detected by samtools (mpileup) and further filtered by the known SNPs.7222-172064 SNPs were detected from the sequenced samples. Among them,we focused on the SNPs with 20 or more reads. The olfactory receptor genes,known to be monoallelically expressed, were confirmed to be monoallelic in oursamples. Some genes contained mix of monoallelic and biallelic SNPs indifferent exons, suggesting that specific exons are monoallelically expressed.More monoallelic SNPs were found in samples with higher sequencing coveragethan those with lower coverage, suggesting that monoallelic genes tend to beexpressed at lower levels when compared to biallelic genes.Our data indicates widespread monoallelic genes in the olfactory neurons. Wehypothesize that complex epigenetic regulation at the allele level is operated inthe nervous system.Ming-Shan Chien International Institute for Advanced Studies Research Conference 2011mingshan.chien@duke.eduPoster PresentationLaboratory of Hiroaki MatsunamiDuke University Medical Center252 CARL, Research Drive, Durham NC 27710EducationCurriculum VitaeDuke University (Aug. 2008 -- Present) – Graduate student• Developmental biology and stem cell program (Aug. 2008 – Present)• University Program in Genetics and Genomics(Aug. 2009 – Present)• 1st rotation project– Functional analysis of OR7D4s in different primates (Hiroaki Matsunami’s lab)• 2nd rotation project– Wnt signaling in epidermal patterning of Drosophila embryos (Amy Bejsovec’s lab)• 3rd rotation project– Specific marker genes exploration for different cell-type cortex neurons (Fan Wang’s lab)National Taiwan University (Feb. 2004 – Jan. 2006) – M.S., Institute of Zoology• Overall GPA : 4.00/4.00• Thesis: Molecular cloning, expression and functional analyses of citron kinase in zebrafish embryos.• Poster: 45th Annual Meeting of the American Society for Cell Biology, San Francisco, United State, 2005• The Memory of Hsieh, Te-Kui and Feng, Sung-Yen Scholarship• The Scholarship of the Neurobiology and Cognitive Science CenterNational Taiwan University (Sep. 1999 – Jan. 2004) – B.S., Department of Horticulture Science– B.S., Department of Life Science (formerly Zoology)• Summer Student Project (Jun. 2002 – Sep. 2002) – The effects of carbohydrate on the growth and regenerationefficiency from embryogenic callus cultures of Oncidium ‘Gower Ramsey’ (Peng-Lin Huang’s lab)• Undergraduate Research Program (Jul. 2003 – Jan. 2004) – The effects of Microcystin-LR, a cyanobacterial toxin,on zebrafish embryonic development. (Shyh-Jye Lee’s lab)Work Experience• Part-time Amanuensis for Journal of the Taiwan Society for Horticultural Science (Sep. 2000 – Jun. 2002) Department of Horticulture Science, National Taiwan University. (Iou-Zen, Chen’s lab)• Research Assistant at (Mar. 2006 – May. 2008) Institute of Biomedical Science, Academia Sinica, Taipei, Taiwan. (Tang K, Tang’s lab) Projects – The checkpoint regulation of kinetochore molecules during meiosis.– The effects of centrosomal proteins on the development of neuron.Publication1. Zh uang, H, M.S. Chien, H. Matsunami. 2009. Dynamic functional evolution of an odorant receptor forsex-steroid-derived odors in primates. Proc Natl Acad Sci. 106(50):21247-512. Chien, Ming-Shan. 2006. Molecular cloning, expression and functional analyses of citron kinase in zebrafishembryos. (Master Thesis, poster in the 45th Annual Meeting of the American Society for Cell Biology, 2005)3. Lee, S.J., C.C. Ju, S.L. Chu, M.S. Chien, T.H.Chan, and W.L. Liao. 2007. Molecular cloning, expression andphylogenetic analyses of parvalbumin in tilapia, Oreochromis mossambicus. J Exp Zool Part A Ecol Genet Physiol.307:51-61.4. Wang, P.J., M.S. Chien, F. J. Wu, H. N. Chou, and S.J. Lee. 2005. Inhibition of embryonic development bymicrocystin-LR in zebrafish, Danio rerio. Toxicon. 45:303-8.19293

Poster PresentersDynamic correlations of local inhibition shape lateDynamic correlations of local inhibition shape latevisual visual responsesPersonal DataCURRICULUM VITAEKenta FunayamaThe University of TokyoAbstractKenta FunayamaThe University of TokyoThe visual cortex responds to spatiotemporally patterned visual stimuli with specificallystereotyped activities; however, less is known about its responses to more featureless,non-patterned stimuli. By patch-clamping layer 2/3 neurons in the mouse primary visualcortex in vivo, we examined visual responses to simple light flashes. A flash stimuluselicited a biphasic response consisting of a rapid, transient depolarization with a latencyof approximately 80 ms (the early response); thereafter, we observed a prolonged, largerName: Kenta FunayamaAddress Correspondence:Laboratory of Chemical Pharmacology,Graduate School of Pharmaceutical Science,The University of Tokyo,7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, JapanEducation and professional training2007 Graduated from International Christian University High School2011 Graduated from Keio University2011~ Ph.D. student at The University of Tokyodepolarization that persisted for a few seconds (the late response). Late responses werecharacterized by a balanced increase in excitatory and inhibitory conductances and wereaccompanied by occasional action potentials. The timing of action potentials waspredominantly determined by intermittent inhibitory barrages, which emerged through atransient coupling of locally correlated inhibitory circuits. Our data suggest that, underbasal conditions, nearby inhibitory interneurons are synchronized, forming patches oflocally correlated inhibition that synchronize more globally in response to a visualstimulus and shape the cortical spike output pattern.9495

Poster PresentersThe Angelman Syndrome protein Ube3Aregulates synapse development and functionby ubiquitinating ArcThe Angelman Syndrome protein Ube3A regulates synapsedevelopment and function by ubiquitinating ArcPaul L. GreerHarvard Medical SchoolPaul L. Greer, Rikinari Hanayama, Caleigh Mandel-Brehm, JohnSalogiannis, Michael E. GreenbergHarvard Medical School, Department of Neurobiology, 220 LongwoodAvenue, Boston, MA, 02115Paul L. GreerHarvard Medical SchoolAngelman Syndrome is a debilitating neurodevelopmental disorder, whichis characterized by ataxia, frequent seizures, and severe mentalretardation. At the time that we initiated these studies, although it wasknown that Angelman Syndrome resulted from mutation of the E3 ubiquitinligase Ube3a, little was known of the role that Ube3a plays during normalnervous system development, or why mutation of Ube3a results in thecognitive impairment underlying Angelman Syndrome. To begin toaddress these questions, we undertook a mass spectrometry-basedscreen to identify substrates of Ube3A in the hope that uncovering Ube3Asubstrates might provide insight into Ube3A's role in nervous systemdevelopment and function. By this approach we identified the protein Arc,whose principal function appears to be regulating the cell surfaceexpression of AMPA receptors, as a neuronal substrate of Ube3a. Theidentification of Arc as a Ube3A substrate led us to hypothesize that AMPAreceptor expression might be impaired in the absence of Ube3A.Consistent with this hypothesis, when compared to wildtype mice, Ube3Amutant mice have significantly reduced AMPA receptor expression andfunction. We further found that this defective AMPA receptor functionresulted from an excessive accumulation of Arc in Ube3A mutantmice. These results suggest that restoring the level of Arc expression tothat which is found in wildtype mice might ameliorate some of thebehavioral deficits that are observed in Ube3A deficient mice, and we haverecently begun mouse genetic experiments aimed at investigating thispossibility. Our preliminary results suggest that restoring Arc levels tothose observed in wildtype mice is sufficient to improve cognitive andmotor function in Ube3A knockout mice, thus suggesting potentialtherapeutic approaches in humans for this previously untreatable disorder.Harvard Medical School220 Longwood AveGoldenson 405Boston, MA 02115EducationPaul Lieberman Greer2008 Harvard Medical School; Boston, MAPh.D. Microbiology and Molecular Genetics2001 Harvard College; Cambridge, MAA.B. Biochemistry magna cum laudeResearch Experience(617) 694-8457 (mobile)(617) 734-7557 (fax)paul_greer@student.hms.harvard.edu2010-present Postdoctoral Fellow; Harvard Medical School, Boston, MAAdvisor: Dr. Sandeep Robert Datta2008-2009 Postdoctoral Fellow; Harvard Medical School, Boston, MAAdvisor: Dr. Michael Greenberg2002-2008 Graduate student; Children’s Hospital, Boston, MAAdvisor: Dr. Michael Greenberg2001 Rotation Student, Harvard Medical School, Boston, MAAdvisor: Dr. Lewis C. Cantley1998-2001 Undergraduate Honors Thesis, Harvard Medical School, Boston, MAAdvisor: Dr. Li-Huei TsaiPublicationsGreer PL, Hanayama R, Bikoff JB, Hong EJ, Greenberg ME. Ube3A restricts synapsenumber by ubiquitinating and degrading Arc. Manuscript in preparation.Margolis SS, Salogiannis J, Lipton DM, Mandel-Brehm C, Willis ZP, Mardinly AR, HuL, Greer PL, Bikoff JB, Ho HY, Soskis MJ, Sahin M, Greenberg ME. Eph-B mediateddegradation of the RhoA GEF Ephexin5 relieves a developmental brake on excitatorysynapse formation. Cell 2010 Oct 29; 143(3):442-55Greer PL, Hanayama R, Bloodgood BL, Flavell SW, Kim TK, Griffith EC, Maehr R,Ploegh HL, Waldon Z, Chowdhury S, Worley PF, Steen J, Greenberg, ME. The9697

Angelman Syndrome-associated ubiquitin ligase, Ube3A, regulates synapse developmentand function through the ubiquitination of Arc. Cell 2010 Mar 5; 140(5):704-16.Greer PL, Hanayama R, Bikoff JB, Hong EJ, Greenberg ME. Ube3A restricts synapsenumber by ubiquitinating and degrading Arc. Manuscript in preparation.Flavell SW, Cowan CW, Kim TK, Greer PL, Lin Y, Paradis S, Griffith EC, Hu LS,Chen C, Greenberg ME. Activity-dependent regulation of MEF2 transcription factorssuppresses excitatory synapse number. Science 2006 Feb 17;311(5763):1008-12.Egea J, Nissen UV, Dufor A, Sahin M, Greer P, Kullander K, Mrsic-Flogel TD,Greenberg ME, Kiehn O, Vanderhaeghen P, Klein R. Regulation of EphA4 kinaseactivity is required for a subset of axon guidance decisions suggesting a key role forreceptor clustering in Eph function. Neuron. 2005 Aug 18;47(4):515-28Cowan CW, Shao YR, Sahin M, Shama SM, Lin MZ, Greer PL, Gao S, Griffith EC,Brugge JS, Greenberg ME. Vav family GEFs link activated Ephs to endocytosis and axonguidance. Neuron. 2005 Apr 21; 46(2);205-17.Sahin M*, Greer PL*, Lin MZ, Poucher H, Eberhart J, Schmidt S, Wright TM, ShamahSM, O’connell S, Cowan CW, Hu L, Goldberg JL, Debant A, Corgas G, Krull CE,Greenberg ME. Eph-dependent tyrosine phosphorylation of ephexin1 modulates growthcone collapse. Neuron 2005 Apr 21;46(2):191-2004Brunet A, Sweeney LB, Sturgill JF, Chua KF, Greer PL, Lin Y, Tran H, Ross SE,Mostoloslavasky R, Cohen HY, Hu LS, Cheng HL, Jedrychowski MP, Gygi SP, SinclairDA, Alt FW, Greenberg ME. . Stress-dependent regulation of FOXO transcription factorsby the SIRT1 deacetylase. Science 2004 Mar 26;303(5666):2011-5Dhavan R*, Greer PL*, Morabito MA, Orlando LR, Tsai LH. The cyclin-dependentkinase 5 activators p35 and p39 interact with the alpha-subunit of Ca2+/calmodulindependentkinase II and alpha actinin-1 in a calcium dependent manner. J. Neurosci.2002; 22(18): 7879-9198

Poster PresentersTransformation from relative timingto firing rate in the central olfactory pathwayTransformation from relative timing to firing rate in thecentral olfactory pathwayRafi HaddadHarvard UniversityRafi HaddadHarvard UniversityRafi Haddad, Anne Lanjuin, Linda Madisen, Hongkui Zeng, Venkatesh Murthy andNaoshige Uchida,*AbstractSensory stimuli elicit neural spiking which carries information from the periphery tothe brain. Traditionally, the overall rate of these spikes has been used to characterizeneuronal responses but accumulating evidence suggests that timing of spikes alsocarries information. However, whether and how downstream neurons decode thesetemporal patterns remains unclear. We addressed this question by optogeneticallystimulating two foci of olfactory nerve inputs or mitral/tufted cells with varying relativetiming, while measuring the spiking activity of downstream neurons. We found that theoverall spike rates of piriform cortex neurons were exquisitely sensitive to relativetiming of input activation. Posterior piriform neurons showed higher sensitivity torelative input times than neurons in the anterior piriform cortex. In contrast, neuronsin the olfactory bulb barely showed such sensitivity. Thus, the brain can transform arelative time code in the periphery into a firing rate-based representation in deeperbrain areas.REFAEL (Rafi) HADDADC U R R I C U L U M V I T A EPost doctoral fellow, Department of Molecular and Cell Biology, Cambridge, MA 02138, USAEducation2009 -Current Postdoctoral fellow at the Molecular and Cellular Biology at HarvardUniversity with Prof. Naoshige Uchida and Prof. Venkatesh Murphy.Project: Using optogenetic tools to resolve odor coding principles andtheir relation to behavior.2006-2009 The Weizmann Institute of Science, combined PhD in appliedmathematics, computer science and neurobiology. (Advisors: Prof.David Harel and Prof. Noam Sobel)2004-2005 The Weizmann Institute of Science, M.Sc in applied mathematics andcomputer science. (Advisors: Prof. David Harel)1993-1996 Tel-Aviv University, B.Sc in applied mathematics and computer science(cum laude), the interdisciplinary excellence program.Papers1. R. Haddad, R. Khan, B. Nadler, N. Mandairon, M. Bensafi, E. Schneidman and N.Sobel; "An Axis-Based Olfactory Neural Code that Predicts Behavior andPerception"; J. Neuroscience, 2010.2. R. Haddad, D. Harel, N. Sobel; "Predicting Odor Pleasantness with anElectronic Nose"; PLoS Computational Biology, 2010.3. R. Haddad, D. Harel, N. Sobel; "Measuring smell"; Current Opinion inNeurobiology, 2008.4. R. Haddad, R. Khan, Y.K. Takahashi, K. Mori, D. Harel and N. Sobel; "A metricfor odorant comparison"; Nature Methods, 2008.5. R. Haddad, L. Carmel, N. Sobel and D. Harel; "Predicting the Receptive Rangeof Olfactory Receptors"; PLoS Computational Biology, 2008.6. R. Khan, C. Luk, A. Flinker, A. Aggarwal, H. Lapid, R. Haddad and N. Sobel;"Predicting Odor Pleasantness from Odorant Structure: Pleasantness as aReflection of the Physical World"; J Neuroscience, 2007.7. R. Haddad, L. Carmel, and D. Harel; "A Feature Extraction Algorithm forMulti-peak Signals in Electronic Noses"; Sensors and Actuators B: Chemical,2007.100101

Poster PresentersDistinct roles of the direct and indirect pathwaysin the Distinct basal roles ganglia of the direct to reward and indirect pathways in theand basal aversive ganglia behavior to reward and aversive behaviorTakatoshi HikidaOsaka Bioscience InstituteTakatoshi HikidaOsaka Bioscience InstituteAbstract: The basal ganglia are the key neural substrates that control motor balance,reward-based and aversive learning. Dysfunction of the basal ganglia leads toneuropsychiatric disorders such as Parkinson's disease, Huntington's disease, depression,schizophrenia, and drug addiction. The striatal projection neurons are GABA-containingmedium-sized spiny neurons (MSNs), which are divided into two subpopulations, i.e.,striatonigral neurons in the direct pathway and striatopallidal neurons in the indirectpathway. The inputs of these two pathways converge at the substantia nigra parsreticulata and control the dynamic balance of the basal ganglia-thalamocortical circuitry.Because the two types of MSNs exist in a similar number and are indistinguishable in size,shape, and basic physiological properties, the different regulatory roles of the twosubpopulations are little understood. We developed a reversible neurotransmissionblocking (RNB) technique, in which transmission-blocking tetanus toxin was specificallyexpressed in the direct striatonigral or the indirect striatopallidal pathway and, in turn,blocked each pathway in a doxycycline-dependent manner. The results indicated that thecoordination of these two pathways was necessary for acute psychostimulant actionselicited by dopamine stimulation. This coordinated modulation, however, shifted to thepredominant role of each pathway in reward-directed and aversive behavior. Blockade ofthe direct pathway selectively impaired rewarding learning and cocaine sensitization. Bycontrast, blockade of the indirect pathway specifically abrogated aversive behavior.These two pathways thus have distinct roles: the direct pathway critical for distinguishingassociative rewarding stimuli from non-associative ones and the indirect pathway forrapid memory formation to avoid aversive stimuli.CURRICULUM VITAEName: Takatoshi HIKIDA, M.D. Ph.D.Present address: Department of Systems Biology, Osaka Bioscience Institute6-2-4 Furuedai, Suita, Osaka 565-0874, JAPANEDUCATION:2002 Ph.D. Department of Biological Sciences, Faculty of Medicine, Kyoto UniversityGraduate School, Kyoto, Japan (mentored by Prof. Shigetada Nakanishi)1997 M.D. Faculty of Medicine, Kyoto University, Kyoto, Japan (research mentors: Profs.Akira Kakizuka & Shuh Narumiya)PROFESSIONAL EXPERIENCE:2011. Oct~ Associate Professor (PI), Kyoto University Faculty of Medicine, Kyoto, Japan2009-Present Researcher (PI), PRESTO, JST2005-Present Research Associate, Department of Systems Biology, Osaka Bioscience Institute, Osaka,Japan (mentored by Director Shigetada Nakanishi)2003-2005 Postdoctoral fellow, Department of Neuroscience. Johns Hopkins University School ofMedicine, Baltimore, MD, USA (mentored by Profs. Solomon H. Snyder & Akira Sawa)2002-2003 Postdoctoral researcher, Department of Biological Sciences. Kyoto University Faculty ofMedicine, Kyoto, Japan (mentored by Prof. Shigetada Nakanishi)1997-1998 Resident, Department of Psychiatry, Kyoto University HospitalLICENSURE: Physician’s License in JapanMEMBERSHIPS: Society for Neuroscience, Japan Neuroscience SocietyAWARDS2011 Japan Neuroscience Society Young Investigator Award2010 Houkatsuno Network Young Investigator Award2009 Hayaishi encourage AwardPUBLICATION LIST:1. Kimura K, Hikida T, Yawata S, Yamaguchi T, Nakanishi S. (2011) Pathway-specific engagement ofephrinA5-EphA4/EphA5 system of the substantia nigra pars reticulata in cocaine-induced responses.Proc Natl Acad Sci U S A, 108 (24): 9981-9986.2. Hikida T, Kimura K, Wada N, Funabiki K, Nakanishi S. (2010) Distinct roles of synaptic transmission indirect and indirect striatal pathways to reward and aversive behavior. Neuron, 66: 896-907.3. Schretlen DJ., Vannorsdll TD, Winicki JM, Mushtaq Y, Hikida T, Sawa A, Yolken RH, Dickerson FB,102103

Cascella NG. (2010) Neuroanatomic and cognitive abnormalities related to herpes simplex virus type 1in schizophrenia. Schizophrenia Research, 118: 224-231.4. Hikida T, Mustafa AK, Maeda K, Fujii K, Saleh M, Barrow RK, Huganir RL, Snyder SH, Hashimoto K,Sawa A. (2008) Modulation of D-serine levels in brains of mice lacking PICK1. Biological Psychiatry,63: 997-1000.5. Hikida T, Jaaro-Peled H, Seshadri S, Oishi K, Hookway C, Kong S, Wu D, Xue R, Andradé M, Tankou S,Mori S, Gallagher M, Ishizuka K, Pletnikov M, Kida S, Sawa A. (2007) Dominant-negative DISC1transgenic mice display schizophrenia-associated phenotypes detected by measures translatable tohumans. Proc. Natl. Acad. Sci. U.S.A. 104: 14501-14506.6. Fujii K, Maeda K, Hikida T, Mustafa AK, Balkissoon R, Xia J, Yamada T, Kawahara R, Okawa M,Huganir RL, Ujike H, Snyder SH, Sawa A. (2006) Serine Racemase Binds to PICK1: PotentialRelevance to Schizophrenia. Molecular Psychiatry, 11: 150-157.7. Kitano T, Matsumura S, Seki T, Hikida T, Sakimura K, Nagano T, Mishina M, Nakanishi S, Ito S. (2004)Characterization of N-methyl-D-aspartate receptor subunits involved in acute ammonia toxicity.Neurochem Int. 44: 83-90.8. Kitabatake Y, Hikida T, Watanabe D, Pastan I, Nakanishi S. (2003). Impairment of reward-relatedlearning by cholinergic cell ablation in the striatum. Proc Natl Acad Sci U.S.A. 100: 7965-7970.9. Hikida T, Kitabatake Y, Pastan I, Nakanishi S. (2003) Acetylcholine enhancement in the nucleusaccumbens prevents addictve behaviors of cocaine and morphine. Proc. Natl. Acad. Sci. U.S.A. 100:6169-6173.10. Nakanishi S, Kaneko S, Hikida T, Watanabe D, Pastan I (2003) Role of synaptic integration ofdopaminergic and cholinergic transmissions in basal ganglia function. International Congress Series1250: 487-492.11. Hikida T, Kaneko S, Isobe T, Kitabatake Y, Watanabe D, Pastan I, Nakanishi S. (2001) Increasedsensitivity to cocaine by cholinergic cell ablation in nucleus accumbens. Proc. Natl. Acad. Sci. U.S.A.98: 13351-13354.12. Kaneko S, Hikida T, Watanabe D, Ichinose H, Nagatsu T, Kreitman RJ, Pastan I, Nakanishi S. (2000)Synaptic Integration Mediated by Striatal Cholinergic Interneurons in Basal Ganglia Function. Science289: 633-637.13. Takebayashi H, Oida H, Fujisawa K, Yamaguchi M, Hikida T, Fukumoto M, Narumiya S, Kakizuka A.(1996) Hormone-induced Apoptosis by Fas-Nuclear Receptor Fusion Proteins: Novel Biological Toolsfor Controlling apoptosis in vivo. Cancer Research 56: 4164-4170.104

Poster PresentersMapping the chemical circuitry of the brain:New neuromodulator sensor revealeddopaminergic gain-control of feeding behaviorby starvation in DrosophilaMapping the chemical circuitry of the brain: Newneuromodulator sensor revealed dopaminergic gaincontrolof feeding behavior by starvation Hidehiko in Drosophila K. INAGAKIHidehiko K. INAGAKICalifornia Institute of TechnologyCalifornia Institute of TechnologyHidehiko K. Inagaki 1,2 , Shlomo Ben-Tabou de-Leon 1,2 , Allan Wong 1,2 , Smitha Jagadish 4 , HiroshiIshimoto 3 , Gilad Barnea 5 , Toshihiro Kitamoto 3 , Richard Axel 1,4 , and David J. Anderson 1,2,*1 Howard Hughes Medical Institute, 2 Division of Biology 156-29, California Institute of Technology,Pasadena, California 91125, USA. 3 Department of Anesthesia and Interdisciplinary Programs in Geneticsand Neuroscience, University of Iowa, 51 Newton Road, Iowa City, IA 52242, USA 4 Columbia UniversityCollege of Physicians and Surgeons 701 West 168 th Street, New York 10032, USA. 5 Department ofNeuroscience, Brown University, Providence, RI, USABehavior cannot be predicted from a neuronal “wiring diagram,” because the braincontains a chemical “map” of neuromodulation superimposed upon its synapticconnectivity map. Neuromodulation changes how neural circuits process information indifferent states, such as hunger or arousal. . In order to understand how neuromodulatorsparticipate in controlling behavior, it is critical to identify the neuronal populations that aremodulated under different behavior states. Here we describe a novel, genetically basedmethod to map, in an unbiased and brain-wide manner, sites of neuromodulation underdifferent conditions in the Drosophila brain. This method reveal that dopamine modulategustatory sensory neurons under the state of hunger. With genetic perturbations, andcalcium imaging we found that the well-known effect of hunger to enhance behavioralsensitivity to sugar is mediated indeed, at least in part, by the release of dopamine ontoprimary gustatory sensory neurons, which enhances sugar-evoked calcium influx. Thesedata reinforce the concept that sensory neurons constitute an important locus for statedependentgain-control of behavior, and introduce a new methodology that can beextended to other neuromodulators and model organisms, as well as to the in vivomapping of GPCR activation in non-neuronal tissues.Hidehiko K. INAGAKIGraduate StudentDavid J Anderson's LabCalifornia Institute of TechnologyPasadena, CA 91125 USAEDUCATIONGraduate School:2007 – present –Division of Biology, California Institute of Technology, CAUndergraduate:2004 – 2007 –Department of Biophysics and Biochemistry, School of Science,University of Tokyo, Japan* GPA: 3.8 out of 4.0, graduated with a dean prize for the top student2003 - 2004 –Science 2, College of Art and Science, University of Tokyo, Japan* Entered first on the listSecondary School:2001 - 2003 –Senior High School at Komaba, University of Tsukuba , Japan* The high school is designated as a Super Science High School.AWARDS & SELECTED ABSTRACTSInagaki HK, Ben-Tabou S, Wong A, Jagadish S, Ishimoto H, Barnea G, Kitamoto T,Axel R, Anderson DJ, in prep, Mapping the chemical circuitry of the brain: dopaminergicgain-control of feeding behavior by starvation in Drosophila.Inagaki HK, Kamikouchi A, Ito K. (2010) Protocol for quantifying sound-sensing abilityof Drosophila melanpgaster. Nat Protoc. 5:26-30.Inagaki HK, Kamikouchi A, Ito K. (2010) Methods for quantifying simple gravitysensing in Drosophila melanpgaster. Nat Protoc. 5:20-25.Kamikouchi A, Inagaki HK, Yorozu S, Ito K. (2009) Application of Drosophila as anintegrative neural model to understand how sound, gravity, an wind information areprocessed in the brain. Tanpakushitsu Kakusan Koso. 54:1817-26.Kamikouchi A*, Inagaki HK*, Effertz T, Hendrich O, Fiala A, Göpfert MC, Ito K.(2009) The Neural Basis of Drosophila Gravity Sensing and Hearing. Nature. 458:165-71.*Equally contribution2003 –Incentive award in the Invention Contest, University of Tokyo2004 –A representative for “Future Creation Fear : International Exhibition for YoungInvestors” ,Tokyo2004 –3rd prize in Project Show for Future Engineers, World Engineer’s Convention2004 , Shanghai, China2006 –A representative of School of Science, University of Tokyo for “Overseas VisitProgram (U.C Berkeley & Stanford University)”2007 –Dean prize, School of Science, University of Tokyo2007 –Nakajima foundation2010 –EMBO prize for presentation106107

Poster PresentersDual roles of OSN-derived Semaphorin-3Fin the olfactory circuit formationDual roles of OSN-derived Semaphorin-3F in the olfactory circuit formationKasumi Inokuchi, Haruki Takeuchi, Mari Aoki, Kouichirou Kajikawa & Hitoshi SakanoKasumi InokuchiThe University of TokyoCURRICULUM VITAEName: Kasumi InokuchiWork address: Department of Biophysics & Biochemistry, Graduate School of Science, TheUniversity of Tokyo, Yayoi 2-11-16, Bunkyo-ku, Tokyo 113-0032Email address: kasumi0125@hotmail.comTelephone: +81-3-5841-4397; Fax: +81-3-5689-7240Department of Biophysics and Biochemistry, Graduate School of Science, The University of Tokyo, JapanIn the mouse olfactory system, olfactory sensory neurons (OSNs) project their axons tospecific glomeruli in the olfactory bulb (OB), and creating an olfactory map.Second-order neurons, mitral/tufted (M/T) cells, innervate their dendrites to specificglomeruli and send their axons to the olfactory cortex, transferring the olfactory mapinformation from the OB to higher brain centers. Surgical and genetic studies havedemonstrated that axon-derived guidance molecules alone could organize a coarseolfactory map by axon-axon interactions of OSNs. Although the map topography isestablished independently from the target cues, the map needs to be properly connectedwith second-order neuron, M/T cells, to make the olfactory circuit functional. Howare the primary neuron axons and secondary neurons properly aligned for specificsynapse formation between them? Here, we report that OSN-specific knockout ofSemaphorin-3F (Sema3F) disrupts both axonal projection of OSNs and migration ofmitral cells to the ventral region of the OB. It was found that Nrp2-positive M/T cellsare guided to the Sema3F-negative ventral region in the OB, while Nrp2-negative M/Tcells stay in the embryonic OB, a prospective dorsal region in the adult OB. Theseresults suggest a novel strategy for axon wiring and synapse formation in the mouseolfactory system: a common guidance molecule (Sema3F) secreted by early-arrivingdorsal OSN axons, guides both late-arriving primary neuron (OSN) axons and theirpartner secondary neurons (M/T cells) to the ventral region of the OB for their properalignment and synapse formation. Loss of function experiments of Nrp2 revealed thatNrp2-Sema3F signaling also regulates axonal projection of Nrp2-positive mitral cellsthat target to the medial amygdala. Repeated use of the same pair of guidancemolecules may be a general mechanism for the neural circuit formation in the brain.Education:2005 B.S. in Molecular BiologyTokyo University of Science, Japan2007 M.S.in Molecular Biology (Mentor: Dr. Hitoshi Sakano)The University of Tokyo, JapanThesis: Neural circuit formation in the mouse olfactory systemResearch Experience:2006- Graduate Student, The University of Tokyo, TokyoPublication ListTakeuchi H*, Inokuchi K*, Aoki M, Suto F, Tsuboi A, Serizawa S, Matsuda I, Suzuki M,Aiba A, Yoshihara Y, Fujisawa H and Sakano H (2010) Sequential arrival and gradedsecretion of Sema3F specify the neural map topography at the bulb” Cell, 141(6):1056-67(* contribute equally)108109

Poster PresentersFunctional spike synchrony has significantlylarger onset latency than anatomical spikesynchrony in the cat lateral geniculate nucleus110Hiroyuki ItoKyoto Sangyo UniversityFunctional spike synchrony has significantly larger onset latency than anatomical spike synchrony in thecat lateral geniculate nucleusHiroyuki Ito, Pedro E. Maldonado and Charles M. GrayDepartment of Computer Science and Engineering, Kyoto Sangyo Univ., Kyoto 603-8555, JapanInstituto de Ciencias Biomédicas., Facultad de Medicina, Univ. de Chile, Santiago, ChileCenter for Computational Biology, Montana State Univ., Bozeman, USAPrecisely synchronized neuronal activity has been commonly observed in the mammalian visual pathway(retina, thalamus and cortex) under a wide range of stimulus conditions. Analysis of this neural behaviorhas often assumed that synchronous firing is stationary and maintained throughout the period of visualstimulation. We tested this assumption by applying the method of Unitary Events Analysis to pairs ofsimultaneously recorded spike trains in the cat lateral geniculate nucleus (LGN) that were stimulated withstationary spots of light. To evaluate the significance of synchronous spike events, we developed andapplied a non-parametric bootstrap test. The analysis showed that about half of the single unit pairs(96/195, 49%) displayed significant synchronous activity (unitary events). Some unit pairs displayinghighly transient unitary events failed to show significant synchrony when analyzed with conventionalcross-correlation analysis. In many unit pairs, the unitary events were optimally characterized at a binwidth of 1 ms, indicating that neural synchrony has a high degree of temporal precision. Synchronousfirings in some unit pairs changed their characteristics under different stimulus context (ON/OFF orstationary spots/moving bar). We also examined the temporal modulation of synchronous firing byanother novel bootstrap test and found that half of the unit pairs (46/96, 48%) displayed non-stationarychanges in synchrony that could not be predicted by the modulation of firing rates. Those dynamicssuggest that synchronous firings in the LGN are functional and are not originated from the anatomicaltransmission time difference between the retinal inputs to the two relay cells. This conclusion is supportedalso by another observation: the anatomical synchronies between the retinal afferent (S-potential) and therelay cell had significantly smaller onset latency than the adjacent (intra-tetrode) relay cell pairs.Furthermore, onset latencies were significantly longer in the distant (inter-tetrode, separated by 0.5mm)relay cell pairs than the adjacent relay cell pairs. Irrespective of short onset latency of the firing rates,synchrony in some of distant unit pairs showed a transient increase with a very long latency (300-500ms)after the stimulus presentation. These findings demonstrate that stimulus-evoked synchronous activitywithin the LGN is highly non-stationary and modulated by endogenous processes that are not tightlycorrelated with firing rate.Sex: MaleCURRICULUM Date of birth VITAE : 4 July, 1960Place of birth : Shizuoka, JapanName, Marital Family status name: : Ito MarriedNationality Forename : Japanese HiroyukiSex Present address: Male Department of Intelligent Systems, Faculty of Computer Sciences andDate of birth : Engineerings, 4 July, 1960 Kyoto Sangyo University, Kita-ku, Kyoto 603, JAPAN.Place Education of birth : Shizuoka, : JapanMarital 1979 (April) status - 1983 (March) : Married Department of Physics, Faculty of Sciences, University of TokyoNationality : Japanese Awarded the degree of BSc in physicsPresent 1983 (April) address - 1985 (March) : Department Department of Intelligent of Physics, Systems, Faculty Faculty of Sciences, of Computer University Sciences of and TokyoEngineerings, Awarded Kyoto the Sangyo degree University, of MSc in physics Kita-ku, for Kyoto a thesis 603, entitled JAPAN.Education : "Soliton and Phonons in Polyacetylene and their Optical Properties"1979 (April) - 1983 (March) Department Work supervised of Physics, by Professor Faculty Yasushi of Sciences, Wada University of Tokyo1985 (April) - 1988 (March) Awarded Department the of degree Physics, of BSc Faculty in physics of Sciences, University of Tokyo1983 (April) - 1985 (March) Department Awarded the of degree Physics, of Ph.D. Faculty in of physics Sciences, for a University thesis entitled of TokyoAwarded "Metastability, the degree Adaptability of MSc and in physics Memory for in a Charge thesis entitled Density Waves"Work "Soliton supervised and Phonons by Professor in Polyacetylene Yasushi Wada and their Optical Properties"Research and professional experience: Work supervised by Professor Yasushi Wada1985 1988 (April) - 1989 1988 (March) Department Research Institute of Physics, for Fundamental Faculty of Sciences, Physics, Kyoto University University of TokyoAwarded A fellowship the degree of the Japan of Ph.D. Society in physics for the for Promotion a thesis entitled of Science for Japanese"Metastability, Junior Scientists Adaptability and Memory in Charge Density Waves"Work Research supervised adviser: by Professor Hajime Yasushi Takayama WadaResearch 1989 (April) and - professional 1989 (December)Department experience: of Physics, Kyoto University1988 (April) - 1989 (March) Research A fellowship Institute of the for Japan Fundamental Society for Physics, the Promotion Kyoto University of Science for JapaneseA Junior fellowship Scientists of the Japan Society for the Promotion of Science for JapaneseJunior Research Scientists adviser: Professor Yoshiki Kuramoto1990 (January) - 1992 (March) Research Center for adviser: Nonlinear Professor Dynamics Hajime in Physiology Takayama and Medicine, Department of1989 (April) - 1989 (December)Department Physiology, McGill of Physics, University Kyoto UniversityPost-doctoral A fellowship of fellow the Japan Society for the Promotion of Science for Japanese[1991(July) Junior Scientists - 1992 (March), Research Fellowship of Heart and StrokeResearch Foundations adviser: of Canada] Professor Yoshiki Kuramoto1990 (January) - 1992 (March) Research Center for adviser: Nonlinear Professor Dynamics Leon in Glass Physiology and Medicine, Department of1992(April) - 1995(March) Department Physiology, McGill of Information University and Communication Sciences, Kyoto SangyoPost-doctoral University fellow[1991(July) Lecturere - 1992 (March), Research Fellowship of Heart and StrokeFoundations of Canada][1994(Febrary)-1995(January)Center for Neurosciences, University of California, Davis, USAVisiting Professor]1995(April) - 2000(March) Department of Information and Communication Sciences, Kyoto SangyoUniversityAssociate Professor2000(April) - 2008(March) Department of Information and Communication Sciences, Kyoto SangyoUniversity 111Professor

1995(April) - 2000(March)2000(April) - 2008(March)2008(April) -Department of Information and Communication Sciences, Kyoto SangyoUniversityAssociate ProfessorDepartment of Information and Communication Sciences, Kyoto SangyoUniversityProfessorDepartment of Intelligent Systems, Kyoto Sangyo UniversityProfessorH. ItoThinking about Brain-Machine-Interface -a personal view-. Dynamic Brain Forum 2009, Atami, Japan,March 2, 2009. invited talk.Y. Maruyama and H.ItoCorrelated trial variabilities of multineuron data in visual cortex and their orientation dependences.Neuroscience Research, vol.59, O1-I09, Supplement, (2008). (oral presentation)H.Ito, PE.Maldonado and CM. GrayDynamics of stimulus-evoked spike timing correlations in the cat lateral geniculate nucleus,Neurosci. Abstr., #459.20 (2008). (poster presentation)Soc.Awards :Human Frontier Science Program Long-term Research Fellowship (1993)(awarded, but declined for administrative reason)Paper award, Japanese Neural Network Society (1997)Membership of academic societies:Japan Neuroscience SocietyJapanese Neural Network SocietySociety for NeurosciencePublications: see attached listH.Ito, PE. Maldonado and CM. GrayDynamics of stimulus-evoked spike timing correlations in the cat lateral geniculate nucleus. J.Neurophysiol., 104, 3276-3292 (2010).H. Ito, PE. Maldonado and CM. GrayDynamics of stimulus-evoked spike timing correlations in the cat lateral geniculate nucleus. Neurosci.Research, O1-8-3-4, Supplement, (2010). (oral presentation)Y. Maruyama and H.ItoWhich electrode array samples orientation tuned cells more homogeneously in cat visual cortex,Neurosci. Abstr., #366.12 (2008). (poster presentation)H.ItoResource project on data analysis of multineuronal spike data in Japan.1st INCF workshop on time series data: analysis and management,Stockholm, December 4-5, 2008. invited talk.H.ItoBootstrap significance test of synchronous spike events - A case study of oscillatory spike trains -,Statistics in Medicine, vol.26, 3976-3996 (2007).H.ItoNon-stationary dynamics of synchronous oscillatory spike events in the LGN -Bootstrap significance test-,Neuroscience Research, vol.58, Supplement, O2P-C08, S55 (2007). (oral presentation)Y. Maruyama and H.ItoDevelopment of an electrode array for a homogeneous sampling of orientation tuned cells in the visualcortex, Neuroscience Research, vol.58, Supplement, P2-F35, S161 (2007). (poster presentation)Soc.Y. Maruyama and H. ItoCorrelated trial variabilities between single units in the cat visual cortex –stimulus dependence and itsrelation with the firing rate tuning–.Neuroscience Research, P3-h25, Supplement, (2010). (poster presentation)H. Ito, PE. Maldonado and CM. GrayFunctional spike synchrony has significantly larger onset latency than anatomical spike synchrony in thecat lateral geniculate nucleus.Soc. Neurosci. Abstr., 532.10 (2010) (oral presentation)Y. Maruyama and H. ItoStimulus dependence of correlated trial variabilities and its relation with the rate tuning in the cat visualcortex.Soc. Neurosci. Abstr., 73. 19/003 (2010) (poster presentation)H. ItoThinking about Brain-Machine-Interface -a personal view-. Dynamic Brain Forum 2009, Atami, Japan,March 2, 2009. invited talk.Y. Maruyama and H.ItoCorrelated trial variabilities of multineuron data in visual cortex and their orientation dependences.Neuroscience Research, vol.59, O1-I09, Supplement, 112 (2008). (oral presentation)113H.Ito, PE.Maldonado and CM. Gray

Poster PresentersVisual Visual experience during locomotion locomotion and TrkBand TrkB signaling signaling promote recovery promote of adult recovery visual cortex fromof adult prolonged visual deprivation cortex from prolonged deprivationMegumi KanekoUniversity of California, San FranciscoAuthors: Megumi Kaneko and Michael P. StrykerDept. of Physiology, University of California San FranciscoMegumi KanekoUniversity of California, San FranciscoDepriving one eye of normal patterned vision during early life causes neurons in the visualcortex to lose responsiveness and visual acuity through the deprived eye (amblyopia). Ifsuch abnormal vision is left uncorrected, recovery of normal visual function is difficult inthe adult, both in humans and in higher mammals, because of limited plasticity in maturecortex. However, recent studies using rodents have shown that recovery of the adult visualcortex after prolonged deprivation can be promoted by visual experience in enrichedenvironment or by various pharmacological manipulations. The recent discovery thatneurons in mouse visual cortex respond with more than 2 times the number of actionpotentials during active locomotion than when still (Niell and Stryker, Neuron, 2010) led usto test whether this enhanced response might facilitate recovery from early-onset, long-termmonocular deprivation (MD). In addition, we examined whether TrkB plays a role in suchrecovery during adulthood, as we have shown it does for recovery during critical period(Kaneko et al, Nature Neuroscience, 2008).C57BL/6 wild type or TrkB-F616A mutant mice were monocularly deprived by eyelidsuture from the beginning of the critical period at P22-24 until ~4 months of age, when webegan chronic optical imaging of the intrinsic signal of cortical activity to measure changesin visual responses. After reinstating binocular vision (BV) by opening the deprived eye,cortical responses to that eye gradually increased over 3 weeks but did not reach the level ofnormally-reared animals. This partial recovery was almost completely inhibited inTrkB-F616A mice treated with 1NM-PP1 to inactivate TrkB kinase. In mice that wereexposed to visual stimuli (VS), either contrast-modulated Gaussian noise (noise) or a squarebar drifting in several different directions, while running freely on a foam ball suspended inair for 3-4 hours each day, intrinsic signal responses increased much faster and to a greaterextent: recovery was already significant by 7 days and reached the normal level within 14days. The degree of this enhancement depended on the match between VS presented duringlocomotion and those used for testing. Either VS alone or locomotion alone caused littleenhancement of recovery. Locomotion + VS at least partially compensated for blockade ofTrkB signaling.We then used extracellular electrophysiological recording in layers 2, 3, and 4 toexamine whether and how response properties of individual neurons improve by reinstatedBV following prolonged MD. Consistent with the global changes in the visual cortex as awhole revealed by intrinsic signal imaging, putative excitatory neurons in mice thatexperienced running + VS either noise or drifting gratings during 7d-BV showed restoredspike rates in response to noise or grating stimuli, respectively. These cells in mice thatexperienced running + grating VS, but not running + noise, also showed improvement inorientation selectivity, the binocular matching of preferred orientation, and acuity. Changesin several physiological characteristics of putative inhibitory neurons after prolonged MDand after 7d-BV demonstrated differences from those in excitatory neurons.These results indicate that recovery of responsiveness from prolonged MD in adult visualcortex requires TrkB kinase activity and is facilitated by exposure to visual stimulationwhile the animal is engaged in active locomotion. This facilitation by visual experienceaccompanies improvement of receptive field properties such as orientation tuning andacuity of individual neurons. These findings suggest that enhanced visual responses duringlocomotion may also account for other treatments that promote recovery in the adult cortex.KANEKO, Megumi, M.D., Ph.D.Department of PhysiologyPhone: (415) 476-1311 (work)University of California, San Francisco(415) 994-6411 (cell)513 Parnassus Ave, HSE-804, POBox 0444San Francisco, CA94143-0444Email: mekaneko@phy.ucsf.edu-----------------------------------------------------------------------------------------------------EDUCATION and PROFESSIONAL TRAINING1989 M.D. Shimane University School of Medicine, Izumo-city, Shimane, Japan1989-1991 Resident, Department of Anesthesiology, Shimane Medical School Hospital1993-1996 Instructor, Department of Anesthesiology, Shimane University Medical School1996- 1997 Visiting Research Associate, Department of Anesthesia and Critical Care, TheUniversity of Chicago, Chicago, IL2003 Ph.D. The University of Arizona, Program in Neuroscience2004-present Postdoctoral Fellow (Advisor: Michael P. Stryker), Department of Physiology,University of California San Francisco, San Francisco, CASELECTED PUBLICATIONSKaneko, M.*, Xie, Y.*, Stryker, M.P., Xu, B. A role for dendritic targeting of BNDF mRNA indevelopment and plasticity in visual cortex. Manuscript submitted (* co-first authors)Kaneko, M.*, Cheetham, C.*, Lee, Y-S., Silva, A.J., Stryker, M.P., Fox, K.D. (2010) Constitutively activeH-ras accelerates multiple forms of plasticity in developing visual cortex. Proc. Nat. Acad. Sci. USA107, 19026-19031. (* co-first authors)Kaneko, M., Stellwagen, D., Malenka, R. C., Stryker, M. P. (2008) TNFα mediates one component ofcompetitive, experience-dependent plasticity in developing visual cortex. Neuron 58, 673-680.Kaneko, M., Hanover, J. L., England, P. M., Stryker, M. P. (2008) TrkB kinase is required for recovery,but not loss, of cortical responses following monocular deprivation. Nature Neuroscience 11, 497-504.Lee, T. T., Levi, O., Cang, J., Kaneko, M., Stryker, M. P., Smith, S. J., Shenoy, K. V., Harris, J. S. (2006)Integrated semiconductor optical sensors for chronic, minimally-invasive imaging of brain function.Conf. Proc. IEEE Eng. Med. Biol. Soc. 1, 1025 – 1028.Cang, J.*, Kaneko, M.*, Yamada, J., Woods, G., Stryker, M. P., Feldheim, D. A. (2005) Ephrin-As guidethe formation of functional maps in the visual cortex. Neuron 48, 577-89. (* co-first authors)Cang, J., Renteria, R. C., Kaneko, M., Liu, X., Copenhagen, D. R., Stryker, M. P. (2005) Development ofprecise maps in visual cortex requires patterned spontaneous activity in the retina. Neuron 48, 797-809.Kaneko, M., Nighorn, A. (2003). Inter-axonal Eph-ephrin signaling may mediate sorting of olfactorysensory axons in Manduca sexta. J Neurosci 23, 11523-11538.Kaneko, M., Mestre, C., Sanchez, E. H., Hammond, D. L. (2000) Intrathecally administered gabapentininhibits formalin-evoked nociception and the expression of Fos-like immunoreactivity in the spinalcord of the rat. J Pharmacol Exp Ther 292, 743-751.John, J. M., Kaneko, M., Hammond, D. L. (1998) Intrathecal bicuculline does not increase formalininducedinflammation. Brain Res 794, 320-324.Saito, Y., Kaneko, M., Kirihara, Y., Sakura, S., Kosaka, Y. (1998) Characterization of tolerance tosomatic and visceral antinociception after continuous epidural infusion of morphine in rats. AnesthAnalg 77, 1340-1345.Kaneko, M., Hammond, D. L. (1997) Role of spinal -aminobutyric acid A receptors in fomralin-inducednociception in the rat. J Pharmacol Exp Ther 282: 928-938.Kaneko, M., Saito, Y., Kirihara, Y., Kosaka, Y. (1994) Pregnancy enhances the antinociceptive effects ofextradural lignocaine in the rat. Br J Anaesth 72: 657-661.Kaneko, M., Saito, Y., Kirihara, Y., Collins, J. G., Kosaka, Y. (1994) Synergistic antinociceptiveinteraction after epidural coadministration of morphine and lidocaine in rats. Anesthesiology 80: 137-150.1114115

Poster PresentersOlfactory pathways involvedin innate fear responsesOlfactory pathways involved in innate fear responsesKunio KondohHoward Hughes Medical Institute, Fred Hutchinson Cancer Research CenterKunio KondohHoward Hughes Medical Institute, Fred Hutchinson Cancer Research Center1Kunio Kondoh, 1 Zhonghua Lu, 2 Bradford B. Lowell, and 1 Linda B. Buck1Howard Hughes Medical Institute, Fred Hutchinson Cancer Research Center, Seattle USA, 2 Beth IsraelDeaconess Medical Center and Harvard Medical School, Boston USAThe mouse olfactory system detects odorants and pheromones as well as predator odors thatstimulate innate fear responses. This suggests that there are genetically defined neuralcircuits within the olfactory system that are involved in innate fear responses to specificolfactory stimuli. The anatomical and molecular characteristics of these circuits arepresently unknown. Odorants are initially detected in the olfactory epithelium (OE) of thenose. In contrast, the vomeronasal organ (VNO) is thought to be specialized for detectingpheromones and other substances that elicit innate responses, including fear. OE signalstravel through the main olfactory bulb to the olfactory cortex, which consists of a number ofdistinct areas, including the piriform cortex and olfactory cortical amygdala. The piriformcortex is thought to be critical for odor perception, but the functions of the other areas are amystery. VNO signals travel through the accessory olfactory bulb to two specific parts of theamygdala ('vomeronasal amygdala') that transmit information to the hypothalamus. Toinvestigate the mechanisms and neural circuits that mediate innate fear responses toolfactory stimuli, we have focused on CRH (corticotropin releasing hormone) neurons in thehypothalamus. These neurons serve as key regulators of physiological responses to fear.To identify neurons that transmit olfactory signals to CRH neurons, we have infected CRHneurons with a conditional 'tracer/reporter' virus that travels retrogradely through chains ofconnected neurons. We have observed virus-infected neurons upstream of CRH neurons inboth the OE and VNO pathways, suggesting that both pathways can transmit signals to CRHneurons. Our results further suggest that CRH neurons are directly connected to thevomeronasal amygdala, but indirectly connected to the olfactory cortex. Within the OEpathway, we have observed infected cells in both the piriform cortex and olfactory amygdala,suggesting the potential involvement of both areas in innate fear responses. Interestingly,while responses to common odorants are reportedly seen throughout the piriform cortex,virus-infected neurons were observed predominantly in the posterior part of this structure,raising the possibility that there is a biased organization of neurons involved in innate fearresponses within the piriform cortex.Name: Kunio KondohAddress correspondence: Fred Hutchinson Cancer Research Center, Division of Basic Sciences,1100 Fairview Avenue North / P.O. Box 19024, A3-020,Seattle, WA 98109-1024 USAEducation2007 Ph.D. Graduate School of Biostudies, Kyoto University, Kyoto, Japan2002 B.Sc. Faculty of Science, Kyoto University, Kyoto, JapanPostdoctoral Training2007-present Postdoctoral fellow at laboratory of Dr. Linda Buck. Division of Basic Sciences, FredHutchinson Cancer Research center, Seattle WA, USA2007 Postdoctoral fellow at laboratory of Dr. Eisuke Nishida. Department of Cell andDevelopmental Biology, Graduate School of Biostudies, Kyoto University, Kyoto, JapanFellowships2009-2011 Japan Society for the Promotion of Science (JSPS) Postdoctoral Fellow for ResearchAbroad2004-2007 Jap an Society for the Promotion of Science (JSPS) Research FellowPublicationsSunadome K, Yamamoto T, Ebisuya M, Kondoh K, Sehara-Fujisawa A, Nishida E. (2011) ERK5regulates muscle cell fusion through Klf transcription factors. Developmental Cell 20(2):192-205.Morimoto H., Kondoh K, Nishimoto S, Terasawa K, and Nishida E. (2007) Activation of a C-terminaltranscriptional activation domain of ERK5 by autophosphorylation. The Journal of BiologicalChemistry 282:35449-35456.Kondoh K, Sunadome K, and Nishida E. (2007) Notch signaling suppresses p38 MAPK activity viainduction of MKP-1 in myogenesis. The Journal of Biological Chemistry 282:3058-3065.Kondoh K, Terasawa K, Morimoto H, and Nishida E. (2006) Regulation of nuclear translocation ofextracellular signal-regulated kinase 5 by active nuclear import and export mechanisms. Molecularand Cellular Biology 26:1679-1690.Kondoh K, and Nishida E. (2007) Regulation of MAP kinases by MAP kinase phosphatases.Biochimica et Biophysica Acta 1773:1227-1237Kondoh K, Torii S, and Nishida E. (2005) Control of MAP kinase signaling to the nucleus.Chromosoma 114:86-91.Ebisuya M, Kondoh K, and Nishida E. (2005) The duration, magnitude and compartmentalization ofERK MAP kinase activity: mechanisms for providing signaling specificity. Journal of Cell Science118:2997-3002.116117

Visualizing Neural Circuits Poster with Presenters Activity-Dependent NuclearImport of a Transcription FactorVisualizing Neural Circuitswith Activity-Dependent Nuclear Importof a Transcription FactorKaoru MasuyamaUniversity of TokyoKaoru Masuyama and Jing W WangUniversity of California, San DiegoabstractKaoru MasuyamaUniversity of TokyoMarking active neuron in behaving animals is important for understanding of complex behaviors.However methods which label active neurons during behavior are limited. Here we present anactivity reporter system dubbed CaLexA (calcium dependent nuclear import of LexA) based onthe mechanism of activity-dependent nuclear import of a transcription factor. Nuclear factor ofactivated T-Cell (NFAT) is a calcium responsive transcription factor. The transport of NFATbetween the nucleus and cytoplasm is regulated by the calcium-dependent protein phosphatasecalcineurin. The basic strategy of the CaLexA system is to express an exogenous transcriptionfactor in specific neural populations and its import into the nucleus upon sustained depolarizationinduces the expression of a reporter gene. We employed two binary expression systems: theGal4/UAS system for expressing the chimeric transcription factor LexA-VP16-NFAT, and theLexA/LexAop system for expressing the GFP reporter.We tested this strategy on odorant receptor neurons (ORNs) and projection neurons (PNs) in theDrosophila olfactory system. Our results showed that fly pheromones excite specific neurons inthe antennal lobe. In this proof-of-concept, we expressed the transcription factor to only ORNs orPNs and asked which neurons respond to the pheromones. Furthermore, we applied this systemto visualize neural circuits underlying complex behaviors. Courtship of male flies exhibits acomplex sequence of behaviors that require multiple sensory inputs. We found a small subset ofneurons in the ventral nerve cord was labeled upon courtship experience. This system usingactivity-dependent expression could be applied to visualize active neurons in different modelorganism after appropriate modifications.Curriculum vitaeName: Kaoru MasuyamaCurrent Affiliation: Department of Complexity Science and Engineering, Graduate School of Frontier Sciences,University of Tokyo 5-1-5 Kashiwanoha, Kashiwa, Chiba, 277-8561, JapanEducation2000/4-2002/3 Graduate School of Science, Nagoya University2002/4-2005/3 Graduate School of Science, Kyoto University2005/3 Ph.D. (Science, Kyoto University)Employment Record2004/4-2006/3 JSPS Research Fellow (Institute for virus research, Kyoto University)2006/4-2007/3 Postdoctoral Fellow (University of California, San Diego)2007/4-2009/3 JSPS Research Fellow (University of California, San Diego)2009/4-2011/4 Postdoctoral Fellow (University of California, San Diego)2011/4- Postdoctoral Fellow (University of Tokyo)Activities in academic societies, affiliations and societiesThe Molecular Biology Society of JapanGenetic Society of AmericaJapan Neuroscience SocietyThe RNA SocietyThe RNA Society of JapanPublication List1. Masuyama K., Zhang Y., Rao Y., and Wang JW., Mapping Neural Circuits with Activity-DependentNuclear Import of a Transcription Factor. (in preparation).2. Root CM., Masuyama K., Green DS., Enell LE., Nässel DR., Lee CH. and Wang JW., A PresynapticGain Control Mechanism Fine-Tunes Olfactory Behavior. Neuron 59, 311–321, 2008.3. Mabuchi N, Masuyama K, and Ohno M., Immunoprecipitation analysis to study protein-RNA interactionsin Xenopus oocytes. RNA-Protein Interaction Protocols, Methods in Molecular Biology. 488, 257-265,2008.4. Taniguchi, I.*, Masuyama K.*, and Ohno, M., Role of purine-rich exonic splicing enhancers in nuclearretention of pre-mRNAs. Proceedings of the National Academy of Sciences of the United States ofAmerica 104, 13684-13689, 2007, *equal contribution (published online before print, August 15, 2007).5. Masuyama K, Taniguchi I, Okawa K, Ohno M., Factors associated with a purine-rich exonic splicingenhancer sequence in Xenopus oocyte nucleus. Biochemical and Biophysical Research Communications359, 580-585, 2007 (published online before print, May 30, 2007) .6. Masuyama, K.*, Taniguchi, I.*, Kataoka, N., and Ohno, M., SR proteins preferentially associate withmRNAs in the nucleus and facilitate their export to the cytoplasm. Genes to Cells 9, 959-965, 2004,*equal contribution.7. Masuyama, K., Taniguchi, I., Kataoka, N., and Ohno, M., RNA length defines RNA export pathway.Genes and Development 18, 2074-2085, 2004 (published online before print, August 16, 2004).8. Nagao, I., Masuyama, K., Obokata, J., In vitro evolution of translational cis-regulatory elements.Endocytobiosis Cell Research 15, 385-389, 2004.118119

Poster PresentersFast, Fast, efficient population population codes codes in olfactory in olfactory cortexcortex through through decorrelation decorrelation and synchronization and synchronizationtoto theta-frequency sniffingtheta-frequency sniffingKeiji MiuraTohoku UniversityK. Miura 1,2 , Z.F. Mainen 3 , N. Uchida 4Keiji MiuraTohoku University1. Graduate School of Information Sciences, Tohoku University, Miyagi, Japan2. PRESTO, JST, Saitama, Japan3. Champalimaud Neuroscience Programme at the Instituto Gulbenkian de Ciência, Oeiras,Portugal4. Center for Brain Science, Department of Molecular and Cellular Biology, HarvardUniversity, Cambridge, MA, USAIn the mammalian olfactory system, stimulus qualities are encoded combinatorially acrosshundreds of channels and stimulus dynamics are dominated by rhythmic active sampling attheta frequency. It is, however, not known what advantages these properties render inneural representation of odors in the central brain areas. Here, we hypothesized that theseconfer efficient and rapid population coding in the olfactory cortex that can facilitate rapidand accurate odor-guided behavior. We recorded from ensembles of neurons in the anteriorpiriform cortex of rats performing an odor mixture categorization task. Odor stimulationevoked rapid and transient burst spiking tightly locked to inhalation onset, and thusphase-locked to the theta cycle. Population decoding analysis showed that the informationconveyed by the spikes in the first theta cycle was sufficient to account for behavioralaccuracy. The efficacy of odor representations was facilitated by the fact that olfactorycortex neurons showed not only independent stimulus tuning but essentially zero noisecorrelations, regardless of proximity, allowing for more efficient encoding over largeneuronal ensembles. While these properties can be partly attributed to the distributedconnectivity of the olfactory system, noise correlations and trial-to-trial variability werealso dependent on active sampling, being minimal during theta-frequency sniffing. Thus,distributed, decorrelated and respiration-locked coding in the olfactory cortex yields anefficient and fast odor code, allowing animals to perform accurate odor discriminationusing the information contained in a single theta cycle.KEIJI MIURAmiura@ecei.tohoku.ac.jpWORK EXPERIENCE2011-, Assistant Professor, Graduate School of Information Sciences, TohokuUniversity2008 - 2011, JST PRESTO c/o Uchida lab, Harvard University2006 - 2008, JSPS Research Fellowship c/o Okada lab, University of TokyoEDUCATION2006, Ph. D, Physics, Kyoto University, Kyoto, JapanAWARDS2006, Research Award , Japanese Neural Network Society2005, Young Researcher Award, Japanese Neural Network Society2005, Outstanding Student Paper Award (NIPS 2005)SELECTED PUBLICATION LIST1. K. Miura, An introduction to maximum likelihood estimation andinformation geometry, Interdisciplinary Information Sciences, 2011, in press.2. M. Oizumi, K. Miura, M. Okada, Analytical investigation of the effects oflateral connections on the accuracy of population coding,Physical Review E.2010;81:0519053. K. Watanabe, H. Tanaka, K. Miura, M. Okada, Transfer Matrix Method forInstantaneous Spike Rate Estimation, IEICE Transactions on Informationand - Systems. 2009;E92-D(7):1362-13684. K. Miura, N. Uchida,A Rate-Independent Measure of Irregularity for EventSeries and Its Application to Neural Spiking Activity, 47th IEEE Conference onDecision and Control, 2008:2006-115. K. Nakada, K. Miura, H. Hayashi, Burst Synchronization and ChaoticPhenomena in two strongly coupled resonate-and-fire neurons,InternationalJournal of Bifurcation and Chaos. 2008;18(4):1249-596. K. Miura, Y. Tsubo, M. Okada, T. Fukai, Balanced excitatory and inhibitoryinputs to cortical neurons decouple firing irregularity from rate modulations.The Journal of neuroscience. 2007 Dec 12;27(50):13802-127. K. Miura, M. Okada, S. Amari, Estimating spiking irregularities underchanging environments. Neural computation. 2006 Oct;18(10):2359-868. K. Miura, M. Okada, Globally coupled resonate-and-fire models, Progress ofTheoretical Physics Supplement. 2006;161:255-259120121

Poster PresentersLight induction causes dynamic alterationin the expression of activity-dependent genesLight induction causes dynamic alteration in the expression ofactivity-dependent in the marmoset genes primary in the visual marmoset cortex primary visualcortexYuki NakagamiNational Institute for Basic BiologyYuki NakagamiNational Institute for Basic BiologyYuki Nakagami, Akiya Watakabe, Tetsuo YamamoriThe visual cortex (V1) is one of the best characterize neocortical areas, yet there would be still manyunrevealed features particularly in primates. We have reported that three genes, OCC1, 5-HT1B and5-HT2A serotonin receptor genes, are selectively express in V1 among the neocortex in macaquemonkeys (Tochitani et al., 2001; Watakabe et al., 2009). In V1 of many species of primates, includingmarmosets, the retino-geniculo-cortical pathways from right and left eyes terminate in distinct alternatingocular dominance columns (ODC). By monocular retinal activity deprivation by TTX injection, weobserved decrease of the signals for these three genes in the deprived ODC.In the marmoset (Callithrix jacchus), ODC had been reported to be present in young animals, butabsent in adults (Spatz, 1989). However, several groups have recently reported that in adult marmosets,the primary visual cortex organized with ODC in layer IVc, being detected by activity-dependentimmediate early gene (IEG) expression, and may act under physiological conditions (Markstahler, 1998;Chappert-Piquemal C, 2001). In order to establish a mode system to analyze the activity-dependentgene expression in marmoset V1, we monocularly injected TTX, kept them in darkness for 24-48 hours,and then exposed to light for 0, 0.5, 2, and 4 hours, to examine the time course of the transcription. Bythis method, we were able to compare the induced and non-induced genes by comparing theneighboring ODC in one tissue from the same animal. We examined the expression patterns ofimmediate early genes (IEGs) such as c-FOS, ARC, ZIF28, and SIK1 in addition to 5-HT1B and 5-HT2Areceptor genes.Under in situ hybridization, IEG expressions were little detected without light induction. Upon lightinduction, however, the expression of each IEG rapidly changed the signal intensity and laminar patternin layers IVa, IVc, V, and VI. For example, c-FOS was strongly expressed in layers II/III, IVa, IVc, and VI,within 30 minutes of stimulus onset, and then disappeared rapidly. ARC was also expressed in layersII/III, IVa, V and VI, at 30 minutes but not in layer IVc. Two hours later, ARC in layer IVc increaseddramatically and decreased again at four hours of induction.In contrast to IEG, the expression of 5-HT1B and 5-HT2A receptor genes were mostly confined tolayer IVc and increased in direct proportion to the length of visual stimuli.We also examined the phosphorylation state of CREB at ser133 by immunohistochemical staining,which is well known to be a key regulator of activity-dependent gene transcription in vitro and in vivo inmany species. To our surprise, after visual stimulation, pCREB signal decreased in layer IVc of theinput-receiving columns (i.e., in a complementary fashion to IEG expressions). In conclusion, ourmonocular induction experiments revealed dynamic regulations of activity-dependent genes inmarmoset V1, which mechanisms may be somewhat different from those previously studied in otherspecies.Curriculum Vitae2000-2004 B.A., Department of engineering, Nagoya University2004-2006 M.S., Department of Biotechnology, School of engineering at Nagoya University2006-2011 Ph D student, Department of Basic Biology, The Graduate University for AdvancedStudies [SOKENDAI]2011- Technical assistant, National Institute for Basic Biology (in preparation for Ph Dthesis)122

Poster PresentersOdorant receptor-derived basal activity regulatesolfactory map formation in mouseOdorant receptor-derived basal activity regulatesolfactory map formation in mouseAi NakashikaThe University of TokyoAi NakashimaThe University of TokyoCURRICULUM VITAEName: Ai NakashimaWork address: Department of Biophysics & Biochemistry, Graduate School of Science,The University of Tokyo, Yayoi 2-11-16, Bunkyo-ku, Tokyo 113-0032Education:Ai Nakashika 1 , Haruki Takeuchi 1 , Daniel R Storm 2 , Hitoshi Sakano 11 Department of Biophysics and Biochemistry, University of Tokyo, Tokyo, 113-0032,2 Department of Pharmacology, University of Washington, Seattle, WA 98195, USAIn the mouse olfactory system, olfactory sensory neurons (OSNs) expressing the sameodorant receptor (OR) species converge their axons into a specific set of glomeruli in theolfactory bulb (OB). A remarkable feature of mammalian olfactory system is that ORmolecules instruct axonal projection of OSNs by regulating the expression levels of axonguidance molecules with OR-derived cAMP. However, it is poorly understood how thecAMP signals are generated in an OR-specific manner during development.Many G protein coupled receptors (GPCRs) are known to possess two differentconformations, active and inactive. Sponteneous conversion between them generates aunique level of basal activity even in the absence of agonists. We assumed that the basalactivity of ORs is responsible for generating cAMP signals that regulate axonal projectionof OSNs. To examine this possibility, we tried to analyze the basal activity mutants ofORs. However, due to the difficulty of functional analyses of ORs in vitro, it has notbeen easy to study a possible role of the basal activity with OR mutants. 2 adrenergicreceptor (2AR) is known to share many functional similarities with ORs, and hasextensively been studied for various functions using mutants. It has been reported that2AR can replace the function of ORs for receptor-instructed axonal projection. Basedon these previous studies, we have generated transgenic mice that express the 2ARmutants in OSNs with altered levels of basal activity. Here we report that activity-highmutations cause the posterior shift of glomeruli, whereas activity-low mutations cause theanterior shift. The basal activity mutants affected the expression levels of Neuropilin-1and Plexin-A1. These results demonstrate that it is the OR-derived basal activity thatregulates axonal projection of OSNs, whose level is uniquely determined by OR species.2008 B.S. in Molecular BiologyThe University of Tokyo, Japan2008- Doctor course in Molecular Biology (Mentor: Dr. Hitoshi Sakano)The University of Tokyo, JapanMajor: Molecular Mechanisms of neural map formation in the mouseolfactory systemResearch Experience:2008- : Graduate Student, The University of Tokyo, TokyoBibliography:1. Nishizumi H, Kumasaka K, Inoue N, Nakashima A, Sakano H (2007)Deletion of the core-H region in mice abolishes the expression of three proximalodorant receptor genes in cis. Proc. Natl. Acad. Sci. U.S.A., 104, 20067-20072 .124125

Poster PresentersHCN channels boost spontaneous firing activityof olfactory HCN channels receptor boost spontaneous neurons firing activity ofthrough olfactory basal receptor activation neurons of through β2 adrenoceptorbasal activation ofβ2 adrenoceptorNoriyuki NakashimaKyoto UniversityNoriyuki Nakashima, Takahiro M. Ishii, Harunori OhmoriNoriyuki NakashimaKyoto UniversityOlfactory receptor neurons (ORNs) undergo continuous turnover throughout life andmaintain an axonal projection map from ORNs to the olfactory bulb. CyclicAMP-signaling is known to affect the olfactory map formation, but the underlyingmechanism is yet unknown. On the other hand, electrical activities affect the synapseconnectivity and axonal projections in many neural networks such as visual, auditoryand also olfactory systems. We here investigated the possible regulation of spontaneousfiring activity of ORNs through hyperpolarization-activated cyclic nucleotide-gated(HCN) channels and endogenous cAMP.We applied extracellular recordings onto slice preparations of the mouse olfactoryepithelium. Inhibition of HCN channels by ZD7288 suppressed the spontaneous activitydose-dependently. The spontaneous activity suppressed by ZD7288 was recovered byfield stimulation that depolarized the membrane. Transgenic mice over-expressingHCN4, one of the predominant subtype in mouse ORNs, showed a higher level ofspontaneous firing than their littermates, while knockdown of HCN4 resulted in thedecrease of the spontaneous firing activity. Then how are HCN channels gated open atrest? Phosphodiesterase inhibitor (rolipram) increased while adenylate cyclase inhibitor(SQ22536) and selective blockers for Gs-coupled beta-2 adrenoceptor (Butaxamine andICI 118,551) markedly decreased the spontaneous activity, indicating that beta-2adrenoceptor (ADRB2) constitutively elevates the basal cAMP levels and maintains thespontaneous activity.These results indicate that HCN channels depolarize the membrane potential of theORNs and boost the spontaneous firing activity under the standing activation of ADRB2.Thus HCN channels in ORNs would show cell-specific gating under the control of theendogenous cAMP levels that may set the spontaneous firing rate as a dynamicguidance cue for olfactory map formation.Noriyuki NakashimaPresent affiliationDepartment of Physiology and Neurobiology, Faculty of Medicine, Kyoto University,Yoshida-Konoe, Sakyo-ku, Kyoto, 606-8501, JapanEducation2001-2007 Faculty of Medicine, Kyoto University (B.S., M.D.)2007-2011 Graduate School of Medicine, Kyoto University (Course completed withoutdegree)Fellowships2008 – 2011 JSPS Research Associate (DC1)2011 – present Global COE Associate FellowPublications1) Takahiro M. Ishii, Noriyuki Nakashima, Harunori Ohmori,Tryptophan-scanning mutagenesis in the S1 domain of mammalian HCN channelreveals residues critical for voltage-gated activation. The Journal of Physiology 579;291-30; 2007 Mar 12) Takahiro M. Ishii, Noriyuki Nakashima, Kenji Takatsuka, Harunori Ohmori.Peripheral N- and C-terminal domains determine deactivation kinetics of HCN channels.Biochem. Biophys. Res. Commun. 359(3); 592-8; 2007 May 29Interests and research techniquesI wonder what realizes an entity called the mind. The brain might be the fundamentalcore unit for the mind. I am currently studying how the neural networks are regulated atthe basal state by applying electrophysiological technique in combination withmolecular biological, histo-anatomical and behavioral analyses.126127

Poster PresentersFKBP52 is a key regulatorof microtubule dynamics and modulatesTAU activities in zebrafishHiroko NakataniFondation Nationale de Gérontologie / Inserm UMR788FKBP52 is a key regulator of microtubule dynamics and modulates TAUactivities in zebrafishHiroko Nakatani, Christopher I. Javis, Béatrice Chambraud, Marcel Tawk andEtienne-Emile BaulieuFKBP52 is a member of FK506 binding protein (FKBP) familly that comprisesintracellular receptors for immunossuppressing drugs such as FK506 andrapamycin. It was originally discovered in our laboratory in 1992 as acomponent of a steroid hormone receptor – HSP90 chaperone complex [1].Interestingly, recent biochemical analysis showed a direct and functionalinteraction between FKBP52, tubulin and the Microtubule Associated Protein,TAU, which leads to tubulin depolymerisation in vitro [2,3]. Here, we study thefunction of the FKBP52 ortholog FKBP4 in neural development in zebrafish andwill investigate its interaction with physiological and pathological TAU in vivo. Aknockdown of FKBP52 leads to axonal outgrowth defects in both primarymotoneurons and Posterior Lateral Line nerve (PLLn). Transmitted ElectronMicroscopy analysis showed a reduction in the number of myelinated axons andmitochondria within axons. Collectively, our results reveal an essential role forFKBP52 in microtubule organization, axonal outgrowth and localization ofaxonal cargos. Moreover, we shall study a functional interaction betweenFKBP52 and pathological forms of TAU in vivo. Effects of several FKBP ligandson neuronal cell biology related to several TAU forms will be analysed. The useof an automated fluorescent microscope enabling phenotypic assays onzebrafish whole embryos in high throughput screening is now being tested.[1] Lebeau MC et al. (1992) J Biol Chem. 267, 4281-4.[2] Chambraud B et al. (2007) FASEB J. 21, 2787-97.[3] Chambraud B et al. (2010) Proc Natl Acad Sci USA. 107, 2658-63.Hiroko NAKATANI, Ph.D.Fondation Nationale de Gérontologie / Inserm UMR788Unité de recherche sur les stéroides et système nerveuxHiroko Hôpital Bicêtre, NAKATANI, Bâtiment Ph.D.PINCUS – secteur MarronFondation 80, rue du Général Nationale Leclerc, de Gérontologie / Inserm UMR788Unité 94267 de Le recherche Kremlin-Bicêtre sur les stéroides Cedex, France et système nerveuxHôpital Phone : Bicêtre, +33 1 49 Bâtiment 59 18 73PINCUS – secteur Marron80, E-mail rue : du hiroko.nakatani@upmc.frGénéral Leclerc,94267 Born on Le 29th Kremlin-Bicêtre january 1976 Cedex, at Clamart France(France).Phone : +33 1 49 59 18 73E-mail INTERESTS : hiroko.nakatani@upmc.frBorn Developmental on 29th january neurobiology 1976 at in Clamart mouse (France).& zebrafish.INTERESTSCARRIERSDevelopmental 2011- Postdoctoral neurobiology fellow, Etienne-Emile in mouse & zebrafish.Baulieu Lab, FNG / INSERM U788, France.2006-2011 Postdoctoral fellow, Carlos Parras Lab, CRICM / INSERM U975, France.CARRIERS2003-2006 Postdoctoral fellow, Jean-Pierre Changeux Lab, Institut Pasteur, France.2011- 2003 Ph.D. Postdoctoral Hitoshi fellow, Sakano Etienne-Emile Lab, The University Baulieu of Lab, Tokyo, FNG Japan. / INSERM U788, France.2006-2011 2000 B.S. Hitoshi Postdoctoral Sakano fellow, Lab, The Carlos University Parras Lab, of Tokyo, CRICM Japan. / INSERM U975, France.2003-2006 Postdoctoral fellow, Jean-Pierre Changeux Lab, Institut Pasteur, France.2003 PUBLICATIONS Ph.D. Hitoshi Sakano Lab, The University of Tokyo, Japan.2000 Binder B.S. E, Hitoshi Rukavina Sakano M, Hassani Lab, The H, University Weber M, of Nakatani Tokyo, Japan.H, Reiff T, Parras C, Taylor V, Rohrer H.(2011). Peripheral nervous system progenitors can be reprogrammed to produce myelinatingPUBLICATIONSoligodendrocytes and repair brain lesions. J. Neurosci. 31(17), 6379-6391.Binder E, Rukavina M, Hassani H, Weber M, Nakatani H, Reiff T, Parras C, Taylor V, Rohrer H.(2011). Tolu S, Peripheral Avale ME, nervous Nakatani system H, Pons progenitors S, Parnaudeau can be reprogrammed S, Tronche F, to Vogt produce A, Monyer myelinatingH, Vogel R, deoligodendrocytes Chaumont F, Olivo-Marin and repair brain JC, Changeux lesions. J. JP, Neurosci. Maskos 31(17), U. (2010). 6379-6391.A versatile system for the neuronalsubtype specific expression of lentiviral vectors. FASEB J. 24(3), 723-30.Tolu S, Avale ME, Nakatani H, Pons S, Parnaudeau S, Tronche F, Vogt A, Monyer H, Vogel R, dePuverel Chaumont S, Nakatani F, Olivo-Marin H, Parras JC, C, Changeux and Soussi-Yanicostas JP, Maskos U. N. (2010). (2009). A versatile Prokineticin system receptor for the 2 neuronalsubtype expression specific identifies expression migrating of lentiviral neuroblasts vectors. and their FASEB subventricular J. 24(3), 723-30. zone transient amplifyingprogenitors in adult mice. J. Comp. Neurol. 10:512(2), 232-42.Puverel S, Nakatani H, Parras C, and Soussi-Yanicostas N. (2009). Prokineticin receptor 2Sugimori expression M, identifies Nagao migrating M, Parras neuroblasts CM, Nakatani and their H, Lebel subventricular M, Guillemot zone transient F, Nakafuku amplifyingM. (2008).Ascl1 progenitors is required in adult for mice. oligodendrocyte J. Comp. Neurol. development 10:512(2), in the 232-42. spinal cord. Development 135(7), 1271-81.Sugimori Molles BE, M, Maskos Nagao U, M, Pons Parras S, Besson CM, Nakatani M, Guiard H, Lebel P, Guilloux M, Guillemot JP, Evrard F, Nakafuku A, Cormier M. A, (2008). Mameli-Ascl1 Engvall is required M, Cloëz-Tayarani for oligodendrocyte I, Nakatani development H, Dufour in N, the Bemelmans spinal cord. AP, Development Mallet J, 135(7), Cazala 1271-81. P, GardierAM, David V, Faure P, Granon S, Changeux JP. (2006). Targeted in vivo expression of nicotinicMolles acetylcholine BE, Maskos receptors U, in Pons mouse S, Besson brain using M, Guiard lentiviral P, expression Guilloux JP, vectors. Evrard J Mol A, Cormier Neurosci. A, 30(1-2), Mameli- 105-Engvall 6.M, Cloëz-Tayarani I, Nakatani H, Dufour N, Bemelmans AP, Mallet J, Cazala P, GardierAM, David V, Faure P, Granon S, Changeux JP. (2006). Targeted in vivo expression of nicotinicacetylcholine Nakatani H, Serizawa receptors in S, mouse Nakajima brain M, using Imai lentiviral T, Sakano expression H. (2003). vectors. Developmental J Mol Neurosci. elimination 30(1-2), of105-ectopic 6. projection sites for the transgenic OR gene that has lost zone specificity in the olfactoryepithelium. Eur. J. Neurosci. 18, 2425-2432.Nakatani H, Serizawa S, Nakajima M, Imai T, Sakano H. (2003). Developmental elimination ofectopic Serizawa projection S, Miyamichi sites for K, the Nakatani transgenic H, OR Suzuki gene M, that Saito has lost M, Yoshihara zone specificity Y, Sakano in the olfactoryH. (2003).Negative epithelium. feedback Eur. J. regulation Neurosci. 18, ensures 2425-2432. the one receptor-one olfactory neuron rule in mouse. Science 302,2088-2094.Serizawa S, Miyamichi K, Nakatani H, Suzuki M, Saito M, Yoshihara Y, Sakano H. (2003).Sengoku Negative feedback S, Ishii T, regulation Serizawa ensures S, Nakatani the one H, receptor-one Nagawa F, olfactory Tsuboi A, neuron Sakano rule H. in (2001). mouse. AxonalScience 302,2088-2094. projection of olfactory sensory neurons during the developmental and regeneration processes.Neuroreport 17, 1061-1066.Sengoku S, Ishii T, Serizawa S, Nakatani H, Nagawa F, Tsuboi A, Sakano H. (2001). Axonalprojection Ishii T, Serizawa of olfactory S, Kohda sensory A, neurons Nakatani during H, Shiroishi the developmental T, Okumura and K, regeneration Iwakura Y, processes. Nagawa F,Neuroreport Tsuboi A, Sakano 17, 1061-1066. H. (2001). Monoallelic expression of the odourant receptor gene and axonalprojection of olfactory sensory neurones. Genes Cells. 6, 71-78.Ishii T, Serizawa S, Kohda A, Nakatani H, Shiroishi T, Okumura K, Iwakura Y, Nagawa F,Tsuboi Serizawa A, S, Sakano Ishii T, H. Nakatani (2001). Monoallelic H, Tsuboi A, expression Nagawa of F, the Asano odourant M, Sudo receptor K, Sakagami gene and axonalJ, Sakano H,Ijiri projection T, Matsuda of olfactory Y, Suzuki sensory M, neurones. Yamamori Genes T, Iwakura Cells. 6, 71-78. Y, Sakano H. (2000). Mutually exclusiveexpression of odorant receptor transgenes. Nat. Neurosci. 3, 687-693.Serizawa S, Ishii T, Nakatani H, Tsuboi A, Nagawa F, Asano M, Sudo K, Sakagami J, Sakano H,Ijiri T, Matsuda Y, Suzuki M, Yamamori T, Iwakura Y, Sakano H. (2000). Mutually exclusiveexpression of odorant receptor transgenes. Nat. Neurosci. 3, 687-693.128129

Cross-modal interaction in Poster learning Presentersstimulus-discriminationCross-modal tasks in a mouse interaction model in learningstimulus-discrimination tasks in a mouse modelAndrei T. PopescuUniversity of CaliforniaAndrei T. PopescuUniversity of CaliforniaAndrei T. Popescu, Angie Kang, Jenkang Tao, Michael R Zhou, Arleen Grewal, Hwei Ee, Mu‐ming PooLearning generalization can be observed when stimuli different than the ones used during trainingproduce the same behavioral response as the original ones (immediate transfer), or lead to the fasterlearning of a new association (far transfer). In an extreme case, training to discriminate stimuli in onemodality allows a faster acquisition of similar discrimination in a different modality (Kehoe & Holt, 1984,Campolattaro et al., 2011). Although the phenomenon of learning transfer has been described andcharacterized in different forms, the neural circuit basis remains largely unknown. Here, we attempt touncover the neural mechanisms by using a mouse model of stimulus discrimination learning. Followinghabituation to head fixation, water‐deprived mice were trained to discriminate two sounds, one secondin duration, and learned that licking right after one of the sounds (conditioned stimulus ‐ CS+, whitenoise) resulted in water delivery while the other sound had no effect (non‐conditioned stimulus ‐ CS‐, 5‐kHz pure tone). Performance on this task was measured as percent of CS+ presentations followed bysuccessful reward delivery. A discrimination score was also calculated based on anticipatory lickingduring the sound presentations, normalizing the difference in anticipatory licking during CS+ and CS‐ tothe total number of anticipatory licks. Both performance and stimulus discrimination increasedconsistently over the ten days of training, reaching high, stable values (≥ 75% and ≥ 0.55, respectively)after the first five sessions. At the end of the auditory training animals started a similar discriminationtask, this time using visual stimuli (4‐Hz white flashing light, paired with lick‐dependent water delivery,‐CS+, vs. continuous white light, no reward ‐ CS‐, both one second duration). Performance on the newauditory task improved at a rate similar to the visual task, reaching values of 78.5 ± 0.1 % on the fifthsession. Surprisingly, however, mice were impaired at discriminating the new visual stimuli, and reacheda discrimination score of 0.6 ± 0.07 only on the tenth day of training. This phenomenon was not specificto the auditory‐visual sequence, and occurred when visual‐training was performed first as well.Interestingly, animals that had low discrimination scores at the end of training on the first task, eitherbeing slow learners, receiving less training – 5 days, or subjected to bilateral injections of dopamine D1antagonist SCH‐23390 in the medial prefrontal cortex (mPFC) were much better at discriminating thesecond set of stimuli than the mice with high discrimination scores at the end of training on the first task.This indicates that learning stimulus discrimination in one sensory modality hinders learning a similarstimulus discrimination in a different modality, and that dopamine signaling in mPFC plays a crucial partin this process. Future work will focus on elucidating the modification of dopamine‐dependent rewardcircuit and its role in cross‐modal interaction in learning.Andrei T. Popescu, MD PhDEducationMCB - University of CA#229 Life Science AdditionBerkeley, CA 94720-3200Phone (510) 643-4576E-mail: popescu@berkeley.edu2003 – 2010 graduate student in the Integrative Neuroscience Program at Rutgers University,Newark NJ, Ph.D. degree2002 – 2003 graduate student in the Neuroscience and Behavior Program at University ofMassachusetts, Amherst MA1995 – 2001 “Carol Davila” University of Medicine and Pharmacy, Bucharest RO, Medical Doctordegree2000 graduated the Specialized First Aid Medical Course at the Emergency Hospital,Bucharest RO1991 – 1995 Computer Science High School, Bucharest RO Analyst‐Programmer; Computer OperatordiplomaProfessional experience2010 – Postdoctoral Fellow, Molecular and Cell Biology Dept., University ofCalifornia, Berkeley2005 – 2007 Teaching Assistant for “Neurobiology” at Rutgers University, Newark NJ2004 Teaching Assistant for “Foundations of Neuroscience” atRutgers University, Newark NJ2003 – 2010 Research: in vitro and in vivo characterization of amygdalafacilitatedlearning2002 – 2003 Teaching Assistant for “Method Inquiry in Psychology” at University ofMassachusetts, Amherst MA: lecturing and student evaluationresponsibilities2002 – 2003 Research: molecular techniques and confocal imaging;role of adhesion molecules in synaptic plasticity2001 – 2002 Lecturer for Cellular and Molecular Biology at “CarolDavila” University of Medicine, Bucharest RO:lecturing and student evaluation responsibilities2000 – 2002 Research: the anti‐apoptotic and neuro‐protective role ofphosphatidic acid (molecular techniques)2001 – 2002 Doctor Practitioner in Clinical Neurology at “Colentina” HospitalBucharest, RO130PublicationsShelly M, Cancedda L, Lim BK, Popescu AT, Cheng PL, Gao H, Poo MM.Semaphorin3A regulates neuronal polarization by suppressing axonformation and 131 promoting dendrite growth. Neuron. Aug11;71(3):433‐46 2011

2001 – 2002 Doctor Practitioner in Clinical Neurology at “Colentina” HospitalBucharest, ROPublicationsShelly M, Cancedda L, Lim BK, Popescu AT, Cheng PL, Gao H, Poo MM.Semaphorin3A regulates neuronal polarization by suppressing axonformation and promoting dendrite growth. Neuron. Aug11;71(3):433‐46 2011Popescu AT, Paré D. Synaptic interactions underlying synchronizedinhibition in the basal amygdala: evidence for existence of twotypes of projection cells. J Neurophysiol. Feb;105(2):687‐96 2011Popescu AT, Saghyan AA, Nagy FZ, Paré D. Facilitation of corticostriatalplasticity by the amygdala requires Ca2+‐induced Ca2+ release inthe ventral striatum. J Neurophysiol. Sep;104(3):1673‐80 2010Popa D, Duvarci S, Popescu AT, Léna C, Paré D. Coherent amygdalocorticaltheta promotes fear memory consolidation during paradoxical sleep.Proc Natl Acad Sci U S A. Apr 6;107(14):6516‐9 2010Popescu AT., Popa D., Pare D. Coherent gamma oscillations couple theamygdala and striatum during learning. Nat Neurosci. May10;12(6):801:807 2009Popa D., Popescu AT, Pare D. Contrasting activity profile of two distributedcortical networks as a function of attentional demands. J Neurosci.Jan 28;29(4):1191‐201 2009Popescu AT, Saghyan AA, Pare D. NMDA‐dependent facilitation ofcorticostriatal plasticity by the amygdala. Proc Natl Acad Sci U S A.Jan 2;104(1):341‐6 2007Likhtik E, Pelletier JG, Popescu AT, Pare D. Identification of basolateralamygdala projection cells and interneurons using extracellularrecordings. J Neurophysiol. Dec;96(6):3257‐65 2006Mathew D, Popescu A, Budnik V. Drosophila amphiphysin functions duringsynaptic Fasciclin II membrane cycling. J Neurosci. Nov 19;23(33):10710‐6 2003Vidulescu C, Popescu AT. Membrane blebbing and apoptotic bodies incerebellar cells. J Cell Mol Med. Jul‐Sep;7(3):330‐1 2003Popescu AT, Vidulescu C, Stanciu CL, Popescu BO, Popescu LM. Selectiveprotection by phosphatidic acid against staurosporine‐inducedneuronal apoptosis. J Cell Mol Med. Jul‐Sep;6(3):433‐8, 2002132

Poster PresentersOdor Codingby a Mammalian Receptor RepertoireOdor Coding by a Mammalian Receptor RepertoireHarumi SaitoThe University of TokyoHarumi SaitoGraduate School of Science The University of TokyoOdor sensing is closely linked to emotion and memory, which enables animals to findfood, identify mates and offspring, and avoid danger ). Since the odorant receptor (OR)was identified in 1991, the logics of odor sensing has been intensively studied. In thepresent study, we attempted to elucidate the fundamental principles of odor coding byOR repertoires. We performed high-throughput screening using our own heterologoussystem (1) and the results provided a basis for translating odorants into receptor neuronresponses (2). Currently, we are focusing on ORs involved in the innate fear response /freezing behavior which are specifically activated by the stimulation of fox odor“2,4,5-trimethylthiazoline (TMT)”. We plan to use this information as a platform forstudying the neural network in the brain.Curriculum VitaeHarumi Saito VMD.Ph.D.Work AddressGraduate School of Science The University of TokyoRoom112, Science Bldg #3, 2-11-16 Yayoi Tokyo Japan 113-0032EducationJuly 1998 Ph.D in Life ScienceBabraham Institute, Dept of Neurobiology, Babraham Cambridge UKMarch 1993 Bachelor in Veterinary MedicineIwate University, Ueda, Morioka, JapanResearch Training5/2009-present Postdoctoral fellowDept. of Biophys. and Biochem.,The University of Tokyo, Graduate School of ScienceBunkyo-ku Tokyo 113-0032 Tokyo JapanMentor Dr. Hitoshi Sakano(Major; Cell Biology, Physiology, Molecular biology)Research involved in the neural network in olfaction9/2006-4/2009 Research ScientistDept of Cell BiologyDuke University, Medical CenterDurham North Carolina 27710 U.S.A.Mentor Dr. Marc G Caron(Major; Cell Biology) Research involved in the signaling ofChimokine Receptor, CCR5 related HIV infection.10/2001-8/2006 Postdoctoral fellowDept of Molecular Genetics and Microbiology,Duke University, Medical CenterDurham North Carolina 27710 U.S.A.Mentor:Dr Hiroaki Matsunami(Major; Cellular and Molecular Biology) Research involved intrafficking and functional study of mammalian odorant receptors)4/2000-9/2001 Postdoctoral fellowDepartment of Anatomy and Neurobiology,Washington University School of Medicine,St. Louis, Missouri, 63308 U.S.A.Mentor:Drs Yi Rao and Jane Y. Wu(Major; Cell Biology) Research involved in the axon guidance andneuronal migration in the olfactory system.11/1998-3/2000 Postdoctoral fellowLab. for Neuronal Recognition moleculesBrain Science Institute, RIKEN,Wako, Saitama, Japan. Metor:Dr Kensaku Mori(Major: Anatomy and Molecular Biology): Research involved inthe neurogenesis of olfactory and vomeronasal sensory neurons.4/1998-11/1998 Research AssistantLab. for Neural Architecture,Brain Science Institute, RIKEN,Wako, Saitama, Japan.Mentor:Dr. Tsutomu Hashikawa.(Major: Anatomy and Cell biology): Research involved in themouse motor nervous system.4/1994-3/1998 Graduate studentLab. of Molecular and Cognitive Neuroscience,Dept. of Neurobiology, The Babraham Institute,Cambridge, U.KMentor:Drs. Barry E..Keverne and Piers.C.Emson(Major: Anatomy and molecular biology): Research involved in theisolation and characterization of the odorant and pheromonereceptors and their transduction cascade.PublicationsSaito H, Mainland JD, Chi Q, Zhuang H , Matsunami H Large-scale Deorphaningof a Mammalian Receptor Repertoire Science signaling 2009 Mar 3;2(60):ra9.Saito H, Kubota M., Roberts RW, Chi Q and Matsunami H. RTP Family MembersInduce Functional Expression of Mammalian Odorant Receptors Cell 2004 vol119:679-91Wong K, Ren XR, Huang YZ, Xie Y, Liu G, Saito H, Tang H, Wen L, Brady-Kalnay SM,Mei L, Wu JY, Xiong WC, Rao Y. Signal transduction in neuronal migration: roles ofGTPase activating proteins and the small GTPase Cdc42 in the Slit-Robo pathway.Cell. 2001 vol 107:209-21.Yamaguchi M., Saito H., Suzuki M., and Mori K. Visualization of neurogenesis in themammalian central nervous system using promoter-green fluorescent protein transgenicmice. Neuroreport. 2000 vol 11:1991-6.Liang F., Hatanaka Y., Saito H., Yamamori T. and Hashikawa T. Differentialexpression of gammma-aminobutyric acid type B receptor-1a and 1b mRNA variants inGABA and non-GABAergic neurons of the rat brain. J. Comp.Neurology Vol416:475-495. 2000Saito H., Mimmack M.L., Keverne E.B., Kishimoto J., and Emson P.C.Gene expressionof olfactory receptors and maturation of olfactory neurons shown by G-protein andN-CAM during development. Dev. Brain Res Vol 110:69-81. 1998Saito H., Mimmack M.L., Keverne E.B., Kishimoto J., and Emson P.C.Isolation ofvomeronasal receptors and their co-localization with specific G-proteinMol. Brain Res.Vol 60 pp215-227..1998.Mimmack M.L., Saito H., Evans G., Bresler M., Keverne E.B., and Emson P.C.A novelsplice veriant of the cell adhesion molecule BIG-2 is expressed in the olfactory andvomeronasal neuroepithelia. Mol. Brain Res. 1997 47:345-350Taniguchi K., Saito H., Okamura M., Ogawa, K.Immunohistochemical demonstration of protein gene product 9.5 (PGP 9.5) in theprimary olfactory system of the rat. Neurosci. Lett., 1993 156:24-26134135

Poster PresentersProteomic analysis of odorantreceptor-associated proteins in sensory axonsProteomic analysis of odorant receptor-associated proteins insensory axonsHitomi SakanoUniversity of WashingtonHitomi Sakano 1 , Kunio Kondoh 1 , Charles A. Greer 2 , Taylor Berry 1 , Monika Deo 1 , KasumiInokuchi 3 , Christine C. Wu 4 , Michael J. MacCoss 5 , and Linda B. Buck 1Hitomi SakanoUniversity of Washington1 Howard Hughes Medical Institute, Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA98109, 2 Department of Neurosurgery and Neurobiology, Yale University School of Medicine, New Haven, CT 06520,3 Department of Biophysics and Biochemistry, University of Tokyo, Tokyo, 113-0032, Japan4 Department of Cell Biology, University of Pittsburgh, Pittsburgh, PA 152615 Department of Genome Sciences, University of Washington, Seattle, WA, 98195The axons of olfactory sensory neurons (OSNs) expressing the same odorant receptor (OR)converge in a few glomeruli at specific locations in the olfactory bulb (OB), forming a topographicglomerular map of OR inputs. The OR expressed by the OSN determines its glomerular target.cAMP signaling downstream of ORs appears to play an important role in glomerular target choice,but it is unclear whether the relevant signaling occurs in OSN cilia, where ORs detect odorants, orelsewhere in the neuron. ORs are also present in OSN axons, raising the possibility that axonalORs are involved in axon guidance. To investigate the role of axonal ORs, we used a combinationof immunoprecipitation with anti-OR antibodies and mass spectrometry to identify OR-associatedproteins in the olfactory epithelium versus OB of neonatal or adult mice. Surprisingly, we found thatGi2, an inhibitory G-protein, co-immunoprecipitates with ORs present in neonatal OSN axonsduring the time of their peak synapse formation in the OB. We also identified additional proteinsimplicated in axon pathfinding in other systems. Furthermore, analysis of Gi2 knockout miceshowed that the absence of Gi2 causes a change in the positions of some OR-specific glomeruli,but not others, consistent with the idea that OR interactions with Gi2 might influence glomerulartarget choice.(Funding:Scholarship Fund)Howard Hughes Medical Institute, National Institutes of Health, ARCS Foundation, PoncinH I T O M I S A K A N Ohitomisa@u.washington.eduOBJECTIVE CLINICALLY APPLICABLE RESEARCH IN NEUROSCIENCEEDUCATION• M.D., Ph.D., Neurobiology & Behavior, MSTP University of Washington, 2001-2010• B.A., Molecular & Cell Biology, emphasis in Immunology, UC Berkeley, 1995-1999.RESEARCH EXPERIENCEGraduate Training2003-2008, Dr. L. Buck, Fred Hutchinson Cancer Research CenterI studied how odorant receptors (OR) guide olfactory sensory neuron axons to precise locations in theolfactory bulb. We are the first to successfully isolate OR protein complexes using anti-OR antibodiesand to sequence them by mass spectrometry. We discovered that an inhibitory G-protein interacts withthe OR. Using knock-out and transgenic mice, we determined that the loss of function of this G-proteinalters the axonal targeting in the bulb.Lab RotationswithDr. L. Buck, Fred Hutchinson Cancer Research Center, 2003, Studied the connectivity of GnRH neuronsin the suprachiasmatic nucleus and possible implications on puberty onset.Dr. R Palmiter, University of Washington, 2002, Studied the behavioral and histological effects ofstimulants on Parkin knock-out mice, a genetic model for early-onset Parkinson’s disease.Dr. D. Storm, University of Washington, 2001, Studied the signaling mechanisms of odorant-stimulatedplasticity of olfactory neurons when postsynaptic trophic signals are withdrawn.1997, 1998, Dr. H. Sakano, Tokyo University, Studied the mutually exclusive expression of odorantreceptor genes.Staff Research Assistant Position1999–2001, Dr. A. Theologis, UC Berkeley, First full genome sequencing of a plant species, A. Thaliana.TEACHING ASSISTANCE EXPERIENCE• Neuropathophysiology: undergraduate course, 2006• Physiology: medical student course, 2005AWARDSARCS fellowship, 2005-2008 and Poncin Scholarship, 2004,2005Individual predoctoral NRSA (1 F30 NS053055-01), 2005-2009CONFERENCESKeystone Symposia on Molecular and Cellular Biology 2009, Poster and AbstractKeystone Symposia on Molecular and Cellular Biology 2007, AbstractWestern Student Medical Research Forum 2002, Oral Presentation and AbstractPUBLICATIONSSakano H, MacCoss MJ, Berry T, Deo M, Inokuch K, Wu C, Plummer N, Birnbaumer L, Buck LB. “Anunexpected role for Gi2 in odorant receptor-directed formation of the olfactory map.” In preparation.Sakano H. Odorant Receptor-Associated Proteins and Axon Pathfinding in the Mouse. Doctoral Dissertation,2008.Watt WC, Sakano H, Lee ZY, Reusch JE, Trinh K, Storm DR. “Odorant stimulation enhances survival of olfactorysensory neurons via MAPK and CREB.” Neuron, 2004 Mar; 41(6): 955-967. PMID: 15046727.Yamada K et al., “Empirical analysis of transcriptional activity in the Arabidopsis genome.” Science, 2003 Oct;302(5646): 842-846. PMID: 14593172.Arabidopsis Genome Initiative. “Analysis of the genome sequence of the flowering plant Arabidopsisthaliana.” Nature, 2000 Dec; 408(6814): 796-815. PMID: 11130711.Theologis A et al., “Sequence and analysis of chromosome 1 of the plant Arabidopsis thaliana.” Nature, 2000Dec; 408(6814): 816-820. PMID: 11130712.Serizawa S, Ishii T, Nakatani H, Tsuboi A, Nagawa F, Asano M, Sudo K, Sakagami J, Sakano H, Ijiri T, Matsuda Y,Suzuki M, Yamamori T, Iwakura Y, Sakano H. “Mutually exclusive expression of odorant receptortransgenes.” Nature Neuroscience, 2000 Jul; 3(7): 687-693. PMID: 10862701.136137

Poster PresentersPhenotypic and molecular heterogeneityof zebrafish lateral line neuronsduring circuit formationPhenotypic and molecular heterogeneity of zebrafishlateral line neurons during circuit formationAkira SatoThe University of TokyoAkira SatoThe University of TokyoAuthorsAkira Sato, Katsushi Yamaguchi, Sumito Koshida, Shuji Shigenobu, Hiroyuki TakedaAbstractA common feature in biological systems is cell-to-cell variability in clonal populationsarising from stochastic biochemical reactions and/or differences in microenvironments.From recent studies using unicellular organisms, stem cells and cancer cells, it issuggested that such non-genetic heterogeneity can play an essential role indevelopment and evolution. However, experimental analyses of developing multicellularorganisms often face difficulties because of their structural and numerical complexity. Inthis study, we adopted the zebrafish posterior lateral line (PLL), a simple sensorysystem comprising a small number of neurons, to analyze cell phenotypes and geneexpression at single-cell resolution.Live imaging of single PLL neurons demonstrated that the individual neurons exhibitextensively diverse behavior and morphologies during circuit formation, and they can bedivided into two groups, leaders and followers. These groups not only exhibited distinctbehaviors but also established different patterns of neural circuit. Furthermore, inhibitingcell-cell interaction through Notch signaling with DAPT treatment altered the proportionof leaders within the PLL ganglion. These results suggest that such phenotypicheterogeneity regulated by cell-cell interaction is important to develop a functionalneural circuit.To elucidate molecular mechanisms regulating the phenotypic heterogeneity, and tounderstand a process of the diversification from a homogeneous population, we areperforming the single-cell gene expression profiling in this system. This analysisrevealed that leaders highly express β-actin and neurod as compared to followers, andthe variety in neurod expression level pre-exists to the differentiation into leaders andfollowers. This suggests that highly expression of neurod in part of PLL neuronsactivates neurogenesis, and these neurons extend their axon early, then, becomeleaders. Our findings may provide novel insights into the mechanisms of neural circuitformation at the single-cell level.CURRICULUM VITAEName: Akira Sato Date of Birth: 8 June 1984Office Address:Laboratory of Embryology, Department of biological sciences,Graduate school of science, University of Tokyo Tel: +81-3-5841-44327-3-1, Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan Email: a_sato@biol.s.u-tokyo.ac.jpResearch:My principle research interests lie in the diversification of neurons in their phenotype and geneexpression at the single-cell level. I am currently investigating how cell-to-cell variation in geneexpression is generated, regulated and utilized during neural circuit formation, using zebrafishlateral line system as a simple model.Education:April 2009 – present Ph.D student, University of TokyoMarch 2009M.S. in BIoloty, University of TokyoMarch 2007B.S. in Biology, University of TokyoExperience:April 2009 – present JSPS Research Fellow‘Analysis of Neural Circuit Formation in the Zebrafish Lateral LineSystem ()’Publication:Single-cell analysis of somatotopic map formation in the zebrafish lateral line system,Developmental Dynamics, 2010, 2058-2065Presentations (selected):August 2011 International Conference on Systems Biology, ‘Phenotypic and molecularheterogeneity of zebrafish lateral line neurons during circuit formation’May 2011 Annual Meeting of the Japanese Society for Developmental Biologists,‘Phenotypic and molecular heterogeneity of zebrafish lateral line neurons duringcircuit formation’November 2010 Annual Meeting of the Japanese Society for Quantitative Biology, ‘Fluctuation incellular phenotypes and gene expression among zebrafish lateral line neurons’May 2010 Joint Meeting of the French and Japanese Societies for Developmental Biology,‘Single-Cell Analysis of Somatotopic Map Formation in the Zebrafish Lateral LineSystem’138139

Poster PresentersHunting for Genes that Regulate Remodelingand Life-long Maintenance of Dendritic ArborsHunting for Genes that Regulate Remodeling andLife-long Maintenance of Dendritic Arbors Kohei ShimonoKyoto UniversityKohei ShimonoKyoto UniversityKohei Shimono, Takafumi Nomura, Tadao Usui, and Tadashi UemuraGraduate School of Biostudies, Kyoto University, JapanNeurons develop distinctive dendritic morphologies to receive and process sensory orsynaptic inputs. Dendritic arbors that are formed in early development are often reorganizedand such arbors of many neuronal types are possibly maintained throughout animal life. Togenetically investigate underlying mechanisms of this remodeling and maintenance in vivo,we have employed dendritic arborization (da) neurons, which exhibit dramatic dendriticpruning and subsequent growth during metamorphosis, as a model system. We firstidentified da neurons in the adult Drosophila abdomen and then clarified developmentalbasis of these adult neurons by tracing origins of those cells back to the larval stage. Weand others also showed that the dendritic arbor of one da neuron, v'ada, exhibited prominentradial-to-lattice transformation in one day after eclosion, and the resultant lattice-shapedarbor persisted throughout adult life.To conduct a MARCM screening efficiently, we expressed FLP recombinase in sensoryorgan precursors (SOPs). By using this ‘SOP-FLP’ system, we isolated several mutants thatdisplayed defects in the remodeling and/or the life-long maintenance of dendritic arbors. Toidentify causative genes for these mutants, we have started employing a next-generationsequencing technique to directly compare whole-genomic sequences of several mutantswith each other, in addition to conventional mapping methods. In this poster, we will discussour on-going screening and mapping.140141

Poster PresentersNeural activity in cortical area V4 underlies fineNeural activity in cortical area V4 underlies finestereoscopic depth perceptionstereoscopic depth perceptionHiroshi M. ShiozakiHiroshi M. ShiozakiOsaka UniversityHiroshi M. ShiozakiOsaka UniversityGraduate StudentLaboratory for Cognitive NeuroscienceGraduate School of Frontier BiosciencesOsaka University, JapanHiroshi M. Shiozaki, Seiji Tanabe, Takahiro Doi, Ichiro FujitaLaboratory for Cognitive Neuroscience, Graduate School of Frontier Biosciences,Osaka University, Toyonaka, Osaka 560-8531, Japan.Primates are capable of discriminating depth with remarkable precision using binoculardisparity. Neurons in area V4 are selective for relative disparity, which is the crucialvisual cue for discrimination of fine disparity. Here, we investigated the contribution ofV4 neurons to fine disparity discrimination. Monkeys discriminated whether the centerdisk of a dynamic random-dot stereogram was in front of or behind its surroundingannulus. We first recorded single-unit responses from V4 while the monkeys wereperforming the task. Neuronal thresholds were higher than the behavioral thresholds onaverage. The most sensitive neurons reached thresholds as low as the psychophysicalthresholds. For subthreshold disparities, the monkeys made frequent errors. The variabledecisions were predictable from the fluctuation in the neuronal responses. Thepredictions were based on a decision model in which each V4 neuron transmits theevidence for the disparity it prefers. We then altered the disparity representationartificially by means of microstimulation to V4. The decisions were systematicallybiased when microstimulation boosted the V4 responses. The bias was toward thedirection predicted from the decision model. Taken together, we suggest that disparitysignals carried by V4 neurons underlie precise discrimination of fine stereoscopic depth.Address: Machikaneyama 1-3, Toyonaka, Osaka, 560-8531, JapanEDUCATIONPh.D. in Engineering, 2011, Graduate School of Frontier Biosciences, Osaka University, Japan(April 2005 – December 2011)B.A. in Mathematics, 2005, Department of Science, Osaka University, Japan (April 2001 –March 2005)PUBLICATIONSShiozaki HM, Tanabe S, Doi T, Fujita I (submitted) “Neural activity in cortical area V4underlies fine disparity discrimination”SELECTED PRESENTATIONS / ABSTRACTSShiozaki HM, Doi T, Tanabe S, Fujita I “Effects of microstimulation in cortical area V4 on finedisparity discrimination” The 34th Annual Meeting of the Japanese Neuroscience Society,O3-D-4-2, Yokohama, Japan, September, 2011Shiozaki H, Motonaga T, Tamura H, Fujita I “Pairwise maximum entropy models explaincorrelated activity of neural populations in the inferior temporal cortex of macaque monkeys”The Society for Neuroscience 40th Annual Meeting, 372.12, San Diego, USA, November, 2010Shiozaki H, Tanabe S, Doi T, Fujita I “Role of macaque area V4 in stereoacuity discrimination:neuronal performance and choice probability.” The Society for Neuroscience 36th AnnualMeeting, 801.4, Atlanta, USA, October, 2006142143

CURRENT POSITION:Professor, Department of Sensory and Cognitive Physiology,Kumamoto University School of MedicinePoster PresentersAn Auditory Field in the Mouse Insular CortexAn Auditory Field in the Mouse Insular CortexWen-Jie SongKumamoto University School of MedicineWen-Jie SongKumamoto University School of MedicineAWARD: Parkinson's Disease Foundation Lillian Schorr Fellowship AwardTakeda Science Foundation Visionary Research Grant AwardThe Naitoh Foundation Research Grant AwardThe Uehara Memorial Foundation Research Grant AwardKumamoto University Research Award 2008, 2011Kumamoto University Teaching Award (undergraduate) 2010Kumamoto University Teaching Award (graduate) 2010PUBLICATIONS:Hiroyuki Sawatari, Makoto Takemoto, Masataka Nishimura, Wen‐Jie SongDepartment of Sensory and Cognitive Physiology, Graduate School of Life Sciences,Kumamoto University School of Medicine, Kumamoto 860‐8556, Japan.Previous research has identified five auditory fields in mouse auditory cortex,including the primary field (AI) and the anterior auditory field (AAF). Using avoltage‐sensitive‐dye‐based imaging technique, here we confirmed theexistence of AI and AAF by examining the tonotopy in each field. Further, weidentified a previously unreported insular auditory field (IAF) located rostral toknown auditory fields. Pure tone evoked responses in IAF exhibited the shortestlatency among all auditory fields at lower frequencies. A rostroventral todorsocaudal frequency gradient was consistently observed in the IAF in allanimals examined. Neither response amplitude nor response duration changedwith frequency in the IAF, but the area of activation exhibited a significantincrease with decreasing tone frequency. Taken together, the current resultsindicate the existence of an IAF in mice, with characteristics suggesting a role inCURRICULUM VITAEWen-Jie SongDepartment of Sensory and Cognitive PhysiologyKumamoto University School of Medicine1-1-1 Honjyo, Kumamoto, JapanEDUCATION:PhD institution: Osaka UniversityPost doc institution: University of TennesseeCURRENT POSITION:Professor, Department of Sensory and Cognitive Physiology,Kumamoto University School of MedicineAWARD: Parkinson's Disease Foundation Lillian Schorr Fellowship Award144Takeda Science Foundation Visionary Research Grant AwardThe Naitoh Foundation Research Grant AwardResearch Articles:Sawatari H, Tanaka Y, Takemoto M, Nishimura M, Song W-J. Identification andcharacterization of an insular auditory field in mice. Eur J Neurosci (in press).Okuda Y, Shikata H, Song W-J. A train of electrical pulses applied to the primaryauditory cortex evokes a conditioned response in guinea pigs. Neurosci Res, 2011,71:103-6.Yamagata K, Senoguchi T, Lu MH, Takemoto M, Karim M, Go C, Sato Y, Hatta, Y,Yoshizawa T, Araki E, Miyazaki J, Song W-J. Voltage-gated K + channel KCNQ1regulates insulin secretion in MIN6 beta-cell line. Biochem Biophys Res Comm 2011,407(3):620-5.Yano M, Watanabe K, Yamamoto T, Ikeda K, Senokuchi T, Lu M, Kadomatsu T,Tsukano H, Ikawa M, Okabe M, Yamaoka S, Okazaki T, Umehara H, Gotoh T, SongWJ, Node K, Taguchi R, Yamagata K, Oike Y. Mitochondrial dysfunction andincreased reactive oxygen species impair insulin secretion in sphingomyelin synthase1 null mice. J Biol Chem 2011,286(5):3992-4002.Saitoh K, Inagaki S, Nishimura M, Kawaguchi H, Song W-J. Spontaneous activityresembling tone-evoked activity in the primary auditory cortex of guinea pigs.Neurosci Res. 2010, 68:107-113.Sugo N, Oshiro H, Takemura M, Kobayashi T, Kohno Y, Uesaka N, Song W-J,Yamamoto N. Nucleocytoplasmic translocation of HDAC9 regulates gene expressionand dendritic growth in developing cortical neurons. Eur J Neurosci, 2010,31:1521-1532.Nishimura M, Shirasawa H, Kaizo H, Song W-J. New field with tonotopic organizationin Guinea pig auditory cortex. J Neurophysiol 2007, 97(1):927-32.Song W-J, Kawaguchi H, Totoki S, Inoue Y, Katura T, Maeda S, Inagaki S, Shirasawa H,Nishimura M. Cortical intrinsic circuits can support activity propagation through anisofrequency strip of the guinea pig primary auditory cortex. Cerebral Cortex16(2006)718-729.Maeda S, Song W-J, Ishii S, Nonlinear and noisy extension of independent componentanalysis: Theory and its application to a pitch sensation model. Neural Computation17(2005)115-144.Otsuka T, Abe T, Tsukagawa T, Song W-J, Conductance-based model of thevoltage-dependent generation of a plateau potential in subthalamic neurons. JNeurophysiol 92(2004)255-264.Shin R-M, Masuda M, Miura M, Sano H, Shirasawa T, Song W-J, Kobayashi K, andAosaki T, Dopamine D4 receptor-induced postsynaptic inhibition of GABAergic145currents in mouse globus pallidus neurons. J Neurosci 23(37) (2003) 11662-11672.Saitoh K, Hattori S, Song W-J, Isa T and Takakusaki K, Nigral GABAergic inhibition

Poster PresentersRegulation of cellular excitability is criticalfor neuronal migrationRegulation of cellular excitability is critical for neuronalmigrationYoshiaki TagawaKyoto UniversityNAME:CURRICULUM Yoshiaki Tagawa VITAEAGE: 41NAME: SEX:Yoshiaki Male TagawaAGE: PRESENT POSITION:41 Assistant ProfessorSEX: MAILING ADDRESS:Male Department of BiophysicsPRESENT POSITION:Assistant Kyoto University Professor Graduate School of ScienceMAILING ADDRESS:Department Kitashirakawa-Oiwake-choof BiophysicsKyoto Sakyo-ku, University Kyoto, Graduate 606-8502 School of ScienceKitashirakawa-Oiwake-choTel: 075-753-4238 Fax: 075-753-4229Sakyo-ku, E-mail: tagawa@neurosci.biophys.kyoto-u.ac.jpKyoto, 606-8502EDUCATION:Tel: 075-753-4238 Fax: 075-753-4229April, 1988-March, 1994Kyoto E-mail: University tagawa@neurosci.biophys.kyoto-u.ac.jpFaculty of MedicineEDUCATION:Awarded the degree of M.D., March, 1994April, 1988-March, 1994-November, 19941997Kyoto Ph.D. student University Faculty of MedicineAwarded Supervisor: the Professor degree of Shigetada M.D., March, Nakanishi 1994April, 1994-November, 1997Ph.D. Department student of Biological SciencesSupervisor: Kyoto University Professor Faculty Shigetada of Medicine NakanishiDepartment Awarded the of degree Biological of Ph.D., Sciences July, 1999PROFESSIONAL EMPLOYMENT: Kyoto University Faculty of MedicineDecember, 1997-March, 1999Assistant Awarded Professor the degree of Ph.D., July, 1999PROFESSIONAL EMPLOYMENT: Department of Biological SciencesDecember, 1997-March, 1999Assistant Kyoto University 146 Professor Faculty of MedicineApril, 1999-September, 2003Department Assistant ProfessorBiological SciencesKyoto Department University of Molecular Faculty and of Medicine System BiologyYoshiaki TagawaKyoto UniversityRegulation of excitability is crucial for both mature and developing neural circuit.Excitability of neurons in the developing cerebral cortex is tightly regulated. Previousstudies have shown that immature cortical neurons such as those during migration areless excitable, mainly due to low-level expression of sodium channels. It is proposedthat hyperexcitability during development has adverse effects on the formation ofcortical circuits; however, how increased cellular excitability affects developmentalprocesses such as migration remains unknown.Here, we examined the effect of hyperexcitability on the development of layer2/3 cortical neurons in vivo. Prokaryotic voltage-gated sodium channel NaChBac, agenetic tool for increasing excitability, was ectopically expressed with a fluorescentmarker (GFP or RFP) in mouse layer 2/3 cortical neurons, and their morphology andelectrophysiological properties were examined. Patch clamp recordings fromfluorescently labeled migrating neurons showed little or no voltage-dependent inwardcurrent in control neurons (expressing only GFP), but large current in NaChBacexpressing neurons. This result suggests that ectopically expressed NaChBac isfunctional in layer 2/3 cortical neurons. NaChBac expressing neurons showed severemigration defects: many neurons were located in the intermediate zone/lower corticallayers at postnatal day 3 (P3) when almost all control neurons already reached the uppercortical layers. Interestingly, migrating neurons expressing NaChBac had dendriticbranches. This result implies that NaChBac expressing neurons start dendrite formationbefore migration is completed. Migration defects were not observed by expression of achannel pore-dead mutant and mutants whose voltage-dependency is positively shifted,suggesting that migration defects were caused by ion channel function of NaChBac.These results together suggest that regulation of cellular excitability is critical forneuronal migration; for proper migration, it may be important to keep cellularexcitability at a low level.CURRICULUM VITAEApril, 1994-November, 1997PROFESSIONAL EMPLOYMENT:December, 1997-March, 1999April, 1999-September, 2003September, 2000-December, 2004March, 2004-SUPPORT:April, 1996-November, 1997September, 2000-September, 2001Ph.D. studentSupervisor: Professor Shigetada NakanishiDepartment of Biological SciencesKyoto University Faculty of MedicineAwarded the degree of Ph.D., July, 1999Assistant ProfessorDepartment of Biological SciencesKyoto University Faculty of MedicineAssistant ProfessorDepartment of Molecular and System BiologyKyoto University Graduate School of BiostudiesPost Doctoral FellowSupervisor: Professor Carla J. ShatzDepartment of NeurobiologyHarvard Medical SchoolAssistant ProfessorDepartment of Biophysics (Tomoo Hirano lab)Kyoto University Graduate School of ScienceResearch Fellowships of the Japan Society for thePromotion of Science for Young ScientistsUehara Memorial Foundation Research FellowshipLICENSE:1994 Japanese Medical License RegistrationPUBLICATION LIST:1. Bando Y, Hirano T, Tagawa Y. Stabilization of membrane potential by KCNK potassiumchannels contributes to neuronal migration in the developing cortex. (in preparation)2. Hayashi Y, Tagawa Y, Yawata S, Nakanishi S, Funabiki K. Spatio-temporal control ofneural activity in vivo using fluorescence microendoscopy. (submitted)3. Mizuno H, Hirano T, Tagawa Y. (2010) Pre-synaptic and post-synaptic neuronal activitysupports the axon development of callosal projection neurons during different post-natalperiods in the cerebral cortex. European Journal of Neuroscience 31, 410-4244. Ageta-Ishihara N, Takemoto-Kimura S, Nonaka M, Adachi-Morishima A, Suzuki K,Kamijo S, Fujii H, Mano T, Blaeser F, Chatila TA, Mizuno H, Hirano T, Tagawa Y, OkunoH, Bito H. (2009) Control of cortical axon elongation by a GABA-driven Ca2+/calmodulindependentprotein kinase cascade. Journal of Neuroscience 29(43), 13720-137295. Tagawa Y, Mizuno H, Hirano T. (2008) Activity-dependent development ofinterhemispheric connections in the visual cortex. Reviews in the Neurosciences 19, 19-286. Mizuno H, Hirano T, Tagawa Y. (2007) Evidence for activity-dependent cortical wiring:Formation of interhemispheric connections in neonatal mouse visual cortex requiresprojection neuron activity. Journal of Neuroscience 27(25), 6760-67707. Tagawa Y, Kanold PO, Majdan M, Shatz CJ. (2005) Multiple periods of functional oculardominance plasticity in mouse visual cortex. Nature Neuroscience 8(3), 380-3888. Tagawa Y, Sawai H, Ueda Y, Tauchi M, & Nakanishi S. (1999) Immunohistological studiesof metabotropic glutamate receptor-subtype 6-deficient mice show no abnormality of retinalcell organization and ganglion cell maturation. Journal of Neuroscience 19(7), 2568-25799. Hashimoto T, Inazawa J, Okamoto N, Tagawa Y, Bessho Y, Honda Y, & Nakanishi S.(1997) The whole nucleotide sequence and chromosomal localization of the gene for humanmetabotropic glutamate receptor subtype 6. European Journal of Neuroscience 9:1226-123510. Masu M, Iwakabe H, Tagawa Y, Miyoshi T, Yamashita M, Fukuda Y, Sasaki H, Hiroi K,Nakamura Y, Shigemoto R, Takada M, Nakamura K, Nakao K, Katsuki M, & Nakanishi S.(1995) Specific deficit of the ON response in visual transmission by targeted disruption ofthe mGluR6 gene. Cell 80:757-76511. Sasai Y, Kageyama R, Tagawa Y, Shigemoto R, & Nakanishi S. (1992) Two mammalianhelix-loop-helix factors structurally related to Drosophila hairy and Enhancer of split.Genes & Development 6:2620-2634147

Pheromone Processing in Fly BrainPoster PresentersPheromone Processing in Fly BrainHirofumi TodaResearch Institute of Molecular PathologyHirofumi TodaResearch Institute of Molecular PathologyEDUCATION AND WORKING EXPERIENCE2010- Postdoctoral fellow at Institute of Molecular Pathology, Vienna, ATSupervisor: Dr. Barry J. Dickson2004-2009 D.Sc. Department of Biological Sciences, Graduate School of Life andHirofumi Toda * , Xiaoliang Zhao * , Tianxiao Liu * and Barry J. Dickson **Research Institute of Molecular Pathology, Dr. Bohrgasse 7, A-1030 Vienna, Austria.Animals need to make a proper decision to find right mates. Drosophila serves as agreat model to study this question because of its rich genetic tools and innate sets ofrobust and well-described mating behavior.The female-specific pheromone 7, 11-heptacosadiene (7, 11-HD) is a potent stimulatorof male courtship, but little is known about the neurons that detect and process thissignal. Here, we identify a set of gustatory neurons that co-express pickpocket 23(ppk23) and fruitless (fru) as candidate sensory neurons for the detection of 7,11-HD.Silencing these neurons with tetanus toxin (TNT) or K+ channel rectifier protein (Kir2.1)reduces male courtship to females, as well as to males that have been perfumed with7,11-HD. Conversely, artificial activation of these neurons with TrpA1, a heat sensitivecation channel, or NaChBaCh, a Na+ channel of bacteria, induces male to court othermale, mimicking the effect of perfuming them with 7, 11-HD. Moreover, extracellularbristle recordings show that these neurons fire upon 7, 11-HD application.These fru+/ ppk23+ neurons send sexually dimorphic projections to the prothoracicganglion in ventral nerve cord. We used the GRASP method to identify three classes offru+ candidate second-order neurons: vAB3, vAB3_2 and dAB2. Activation of vAB3/vAB3_2 induces courtship toward male, mimicking both activation of ppk23+/ fru+neurons and 7, 11-HD exposure. In the future, we will silence these neurons to see ifthey are also required for behavioral responses to 7, 11-HD, and perform physiologicalassays to test their response to this pheromone.PERSONAL DATAName:Address:Supervisor:Hirofumi TODADr. Bohr-gasse 7, A1030 Vienna, AustriaDr. Barry J. DicksonEDUCATION AND WORKING EXPERIENCE148Environmental Sciences, University of Tsukuba, Ibaraki, JapanSupervisor: Dr. Katsuo Furukubo-Tokunaga2004-2009 Visiting graduate student at Beckman Research Institute of the City of Hope, CA,USASupervisor: Dr. Toshifumi Tomoda2002-2004 M.Sc. Department of Biological Sciences, Graduate School of Life andEnvironmental Sciences, University of Tsukuba, Ibaraki, JapanSupervisor: Dr. Katsuo Furukubo-Tokunaga2001-2002 Visiting foreign intern at The Rockefeller University, NY, USASupervisor: Dr. Mary E. Hatten1998-2002 B.Sc. College of Biological Sciences, School of Science, University of1998-2002 B.Sc. College of Biological Sciences, School of Science, University ofTsukuba, Ibaraki, Japan1998-2002 B.Sc. College of Biological Sciences, School of Science, University ofTsukuba, Ibaraki, JapanTsukuba, Ibaraki, JapanAWARDS and FELLOWSHIPSAWARDS and FELLOWSHIPSAWARDS and FELLOWSHIPS2010-present EMBO Long-Term Fellowship2010-present EMBO Long-Term Fellowship2010-present EMBO Long-Term Fellowship2007 Travel award, 56th Fujihara seminar2007 Travel award, 56th Fujihara seminar2007 Travel award, 56th Fujihara seminar2001 Atsushi Kitaueda Memorial Fund for summer intern2001 Atsushi Kitaueda Memorial Fund for summer intern2001 Atsushi Kitaueda Memorial Fund for summer internPUBLICATIONS149

PUBLICATIONS1. Mochizuki H, Toda H, Ando M, Kurusu M, Tomoda T, Furukubo-Tokunaga K. (2011)“Unc-51/ATG1 controls axonal and dendritic development via kinesin-mediated vesicle transportin the Drosophila brain.” PLoS One. 2011 May 12;6(5):e196322. Wairkar, Y., Toda, H., Mochizuki, H., Furukubo-Tokunaga, K., Tomoda, T., and DiAntonio, A.(2009)“Unc-51 controls active zone density and protein composition by downregulating ERKsignaling.” J. Neurosci. Jan 14;29(2):517-28.3. Toda, H., Mochizuki, H., Flores III, R., Josowitz, R., Krasieva, T.B., LaMorte, V.J., Suzuki, E.,Gindhart, J.G., Furukubo-Tokunaga, K., and Tomoda, T. (2008)“UNC-51/ATG1 kinase regulates axonal transport by mediating motor–cargo assembly.” GenesDev. Dec 1;22(23):3292-307.4. Sawamura, N., Ando, T., Maruyama, Y., Fujimuro, M., Mochizuki, H., Honjo, K., Shimoda, M.,Toda, H., Sawamura-Yamamoto, T., Makuch, L.A., Hayashi, A., Ishizuka, K., Cascella, N.G.,Kamiya, A., Ishida, N., Tomoda, T., Hai, T., Furukubo-Tokunaga, K., and Sawa, A. (2008)“Nuclear DISC1 regulates CRE-mediated gene transcription and sleep homeostasis in the fruitfly.” Mol. Pshychiatry Dec;13(12):1138-485. Kato, Y., Kuwabara, T., Warashina, M., Toda, H., and Taira, K. (2001) “Relationship betweenthe activities in vitro and in vivo of various kinds of ribozyme and their intracellular localization inmammalian cells.” J. Biol. Chem. 276,15378-15385.6. Kato, Y., Kuwabara, T., Toda, H., Warashina, M., and Taira, K. (2000)“Supression of BCR-ABL mRNA by various ribozymes in HeLa cells.” Nucleic Acids Symp.Ser. 44, 283-284.150

TSUBOI, AkioPoster PresentersSensory input regulates differentiationof a Sensory specific input subtype regulates of differentiation newborn interneuronsof a specificvia subtype 5T4 glycoprotein of newborn interneurons the mouse via 5T4 olfactory glycoprotein bulbin the mouse olfactory bulbAkio TsuboiNara Medical UniversityAkio TsuboiNara Medical UniversityAkio Tsuboi 1 , Hiroo Takahashi 1 , Nobushiro Nishimura 1 , Kensaku Mori 2 , Peter L Stern 3and Sei-ichi Yoshihara 11Laboratory for Molecular Biology of Neural System, Advanced Medical ResearchCenter, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan2Department of Physiology, Graduate School of Medicine, University of Tokyo, Tokyo113-0033, Japan3CR UK Immunology Group, Paterson Institute for Cancer Research, University ofManchester, Manchester M20 4BX, United KingdomSensory input has been shown to regulate development in a variety of species and invarious structures, including the retina, cortex and olfactory bulb (OB). Within themammalian OB specifically, the development of dendrites in mitral/tufted cells is wellknown to be odor-evoked activity-dependent. However, little is known about thedevelopmental role of sensory input in the other major OB population of theGABAgenic interneurons, such as granule cells and periglomerular cells. Here, weidentified, with DNA microarray and in situ hybridization screenings, a trophoblastglycoprotein gene, 5T4, whose expression in the OB interneurons is dependent onsensory input. 5T4 is a type I membrane protein, whose extracellular domain containsseven leucine-rich repeats (LRR) flanked by characteristic LRR-N- and C-flankingregions, and a cytoplasmic domain. 5T4 overexpression in the newborn OBinterneurons facilitated their dendritic arborization even under the sensoryinput-deprived condition. By contrast, both 5T4 knockdown with RNAi and 5T4knockout with mice resulted in a significant reduction in the dendritic arborization ofOB interneurons. Further, we identified the amino-acid sequence in the 5T4cytoplasmic domain that is necessary and sufficient for the sensory input-dependentdendritic shaping of specific neuronal subtypes in the OB. Thus, these resultsdemonstrate that 5T4 glycoprotein is one of molecules that regulate theactivity-dependent dendritic differentiation of interneurons and the formation offunctional neural circuitry in the OB.Keywords: dendritic arborization, granule cells, olfactory bulb, activity dependent, 5T4glycoproteinCURRICULUM VITAEName: TSUBOI, AkioTitle: ProfessorAffiliation: Lab for Molecular Biology of Neural SystemAdvanced Medical Research Center, Nara Medical University840 Shijo-cho, Kashihara, Nara 634-8521, JapanEducation1976-1980 B.Sc. Microbiology, Faculty of Agriculture, Nagoya University, Japan1980-1982 M.Sc. Microbiology, Faculty of Agriculture, Nagoya University, Japan1988 Ph.D. Microbiology, Faculty of Agriculture, Nagoya University, JapanAcademic and Professional Experience:1982-1991 Research Associate, Faculty of Agriculture, Nagoya University, Nagoya,Japan3/1988-5/1988 Visiting Scientist, Molecular Structural Biology, Max-Planck-Institute forBiochemistry, Martinsried, Germany (Advisor: Prof. W. Baumeister)1989-1994 Postdoctoral Fellow, Department of Molecular Biology, DNAX ResearchInstitute, Palo Alto, CA, USA (Advisor: Dr. N. Arai)7/1994-9/1994 Visiting Scientist, Molecular and Developmental Biology, Institute ofMedical Science, University of Tokyo, Tokyo, Japan (Advisor: Dr. K. Arai)1994-1996 Assistant Professor, Department of Cell Fusion, National Institute for BasicBiology, Okazaki, Japan (Advisor: Prof. H. Sakano)1996-2006 Assistant Professor, Department of Biophysics and Biochemistry,Graduate School of Science, University of Tokyo, Tokyo, Japan (Advisor:Prof. H. Sakano)2006- Professor, Lab for Molecular Biology of Neural System, Advanced MedicalResearch Center, Nara Medical University, Kashihara, JapanAwards and Fellowships:2000-2003 Researcher, Precursory Research for Embryonic Science and Technology(PRESTO) program, Japan Science and Technology Agency (JST)Memberships of Academic Society:The Japan Neuroscience SocietyThe Molecular Biology Society of JapanThe Japanese Biochemical Society1152153

TSUBOI, AkioPUBLICATIONSOriginal Articles:1. Tsuboi A, Imai T, Kato H, Matsumoto H, Igarashi K, Suzuki M, Mori K and Sakano H:Two highly homologous mouse odorant receptors encoded by tandemly linkedMOR29A and MOR29B genes differently respond to phenyl ethers.European Journal of Neuroscience 33: 205-213 (2011).2. Takeuchi H, Inokuchi K, Aoki M, Suto F, Tsuboi A, Matsuda I, Suzuki M, Aiba A,Serizawa S, Yoshihara Y, Fujisawa H and Sakano H: Sequential arrival and gradedsecretion of Sema3F by olfactory neuron axons specify map topography at the bulb.Cell 141: 1056-1067 (2010).3. Takahashi H, Yoshihara S, Nishizumi H and Tsuboi A: Neuropilin-2 is required for theproper targeting of ventral glomeruli in the mouse olfactory bulb.Molecular and Cellular Neuroscience 44: 233-245 (2010).4. Tsuboi A, Miyazaki T., Imai T. and Sakano H: Olfactory sensory neurons expressingclass I odorant receptor genes converge their axons on an antero-dorsal domain ofthe olfactory bulb in the mouse.European Journal of Neuroscience 23: 1436-1444 (2006).List of Participants5. Kobayakawa K, Hayashi R, Morita,K, Miyamichi K, Oka Y, Tsuboi A and Sakano H:Stomatin-related olfactory protein, SRO, specifically expressed in the murine olfactorysensory neurons.The Journal of Neuroscience 22: 5931-5937 (2002).6. Ishii T, Serizawa S, Kohda A, Nakatani H, Shiroishi T, Okumura K, Iwakura Y, NagawaF, Tsuboi A and Sakano H: Monoallelic expression of the odourant receptor gene andaxonal projection of olfactory sensory neurones. Genes to Cells 6: 71-78 (2001).7. Serizawa S, Ishii T, Nakatani H, Tsuboi A, Nagawa F, Asano M, Sudo K, Sakagami J,Sakano H, Ijiri T, MatsudaY, Suzuki M, Yamamori T, Iwakura Y and Sakano H: Mutuallyexclusive expression of odorant receptor transgenes.Nature Neuroscience 3: 687-693 (2000).8. Tsuboi A, Yoshihara S, Yamazaki N, Kasai H, Asai-Tsuboi H, Komatsu M, Ishii T,Seizawa S, Matsuda Y, Nagawa F and Sakano H: Olfactory neurons expressingclosely linked and homologous odorant receptor genes tend to project their axons toneighboring glomeruli on the olfactory bulb.The Journal of Neuroscience 19: 8409-8418 (1999).9. Touhara K, Sengoku S, Inaki K, Tsuboi A, Hirono J, Sato T, Sakano H and Haga T:Functional identification and reconstitution of an odorant receptor in single olfactoryneurons. The Proceedings of the National Academy of Sciences of U.S.A. 96:4040-4045 (1999).10. Tsuboi A*, Nagawa F*, Ishiguro K*, Yoshida Y, Ishikawa A, Takemori T, Otsuka AJ andSakano H (*The first three authors contributed equally to this work): Footprint analysisof the RAG protein recombination signal sequence complex for V(D)J typerecombination. Molecular and Cellular Biology 18: 655-663 (1998).2154

IIAS Research Conference 2011 on“Frontiers in Neuroscience: From Brain to Mind”List of ParticipantsNobutaka HirokawaThe University of Tokyohirokawa@m.u-tokyo.ac.jp[Invited Speakers]David AndersonCalifornia Institute of Technologymancusog@caltech.eduHaruo KasaiThe University of Tokyohkasai@m.u-tokyo.ac.jpLinda BuckFred Hutchinson Cancer Research Centerlbuck@fhcrc.orgSigrun KorschingUniversity of Colognesigrun.korsching@uni-koeln.deJean-Pierre ChangeuxCollège de Francechangeux@pasteur.frHiroaki MatsunamiDuke University Medical Centermatsu004@mc.duke.eduBarry DicksonResearch Institute of Molecular Pathologydickson@imp.ac.atTesturo MatsuzawaKyoto Universitymatsuzaw@pri.kyoto-u.ac.jpMichael GreenbergHarvard Medical Schoolmeg@hms.harvard.edu156 157

Kensaku MoriThe University of Tokyomoriken@m.u-tokyo.ac.jpHitoshi SakanoThe University of Tokyosakano@mail.ecc.u-tokyo.ac.jpKenichi OhkiKyushu Universitykohki@med.kyushu-u.ac.jpNoam SobelWeizmann Institute of Sciencenoam.sobel@weizmann.ac.ilSvante PääboMax Planck Institute for Evolutionary Anthropologypaabo@eva.mpg.deNicholas SpitzerUniversity of California, San Diegonspitzer@ucsd.eduMu-ming PooUniversity of California at Berkeleympoo@uclink.berkeley.eduLisa StowersThe Scripps Research Institutestowers@scripps.eduIvan RodriguezUniversity of GenevaIvan.Rodriguez@unige.chMichael StrykerUniversity of California, San Franciscostryker@phy.ucsf.edu158 159

Keiji TanakaRIKEN Brain Science Institutekeiji@riken.jp[Discussants]Kohei HattaUniversity of Hyogokhatta@sci.u-hyogo.ac.jpKazushige TouharaThe University of Tokyoktouhara@mail.ecc.u-tokyo.ac.jpYukiyasu KamitaniATR Computational Neuroscience Laboratorieskmtn@atr.jpNoriko OsumiTohoku University School of Medicineosumi@med.tohoku.ac.jpNaoshige UchidaHarvard Universityuchida@mcb.harvard.eduTakeshi SakuraiKyoto University Graduate School of Medicinesakurai@tk.med.kyoto-u.ac.jpTetsuo YamamoriNational Institute of Basic Biologyyamamori@nibb.ac.jpYoshihiro YoshiharaRIKEN Brain Science Instituteyoshihara@brain.riken.jp160 161

[Poster Presenters]Mohammad AbdolrahmaniSchool of Frontier Biosciences, Osaka Universitym.abdolrahmani@gmail.comIkuma AdachiKyoto University Primate Research Instituteadachi@pri.kyoto-u.ac.jpMing-Shan ChienDuke Universitymingshan.chien@duke.eduKenta FunayamaThe University of Tokyokenta.funayama913@gmail.comPaul GreerHarvard Medical Schoolpaullgreer@gmail.comRafi HaddadHarvard Universityrafihaddad@gmail.comTakatoshi HikidaOsaka Bioscience Institutehikida@obi.or.jpHidehiko InagakiCalifornia Institute of Technologyhidehiko@caltech.eduKasumi InokuchiThe University of Tokyokasumi0125@hotmail.comHiroyuki ItoKyoto Sangyo Universityhiro@cc.kyoto-su.ac.jpMegumi KanekoUniversity of California San Franciscomekaneko@phy.ucsf.eduKunio KondohHoward Hughes Medical Institute, Division of Basic Sciences,Fred Hutchinson Cancer Research Centerkkondoh@fhcrc.orgKaoru MasuyamaGraduate School of Frontier Sciences, University of Tokyomasuyama@neuro.k.u-tokyo.ac.jpKeiji MiuraTohoku Universitymiura@ecei.tohoku.ac.jpYuki NakagamiNational Institute for Basic Biologyn_yuki@nibb.ac.jpAi NakashimaThe University of Tokyoindigoblue1983@hotmail.co.jpNoriyuki NakashimaFaculty of Medicine, Kyoto Universitynakashima@nbiol.med.kyoto-u.ac.jpHiroko NakataniFondation Nationale de Gerontologiehiroko.nakatani@upmc.frAndrei PopescuUniversity of Californiapopescu@berkeley.eduHarumi SaitoThe University of Tokyosaito004@gmail.com162 163

Hitomi SakanoUniversity of Washingtonhitomisa@yahoo.comAkira SatoThe University of Tokyoa_sato@biol.s.u-tokyo.ac.jpKohei ShimonoGraduate School of Biostudies, Kyoto Universitykshimono@lif.kyoto-u.ac.jpHiroshi M. ShiozakiGraduate School of Frontier Biosciences, Osaka Universityshiozaki@bpe.es.osaka-u.ac.jpWen-Jie SongKumamoto University School of Medicinesong@kumamoto-u.ac.jpSite InformationYoshiaki TagawaGraduate School of Science, Kyoto Universitytagawa@neurosci.biophys.kyoto-u.ac.jpHirofumi TodaInstitute of Molecular Pathologyhirofumitoda@hotmail.comAkio TsuboiNara Medical Universityatsuboi@naramed-u.ac.jp164

Site InformationRoom 2162FClosed AreaClosed Area 1FClosed Area 101 102 103 104 105Sec. 2Room Seminar 1Closed Area 111110109108107106Lecture Hall: Main HallSmoking AreaSec. 1Seminar LoungeFloor Map for General ParticipantsPlease do not enter the closed area.Smoking is allowed only in the smoking area.Smoking Area1. Lecture Hall : Main HallCapacityEquipmentOral presentations and discussions will take place in theLecture Hall.The Hall will be closed after the meeting.* During the Presentations, no audio or visual recording and no photography is allowed.* Please leave your oversized luggage at the cloak desk in Room Seminar 1.* To all speakers, please contact our staff well enough before the start of your presentation using the lunch orother break time to let them know the equipment you will require.Staff will assist with any compatibility issues.2. Lobby : Coffee BreakAbout 100 seatsScreen/Projector /PC(Mac/Window)/Cable MicrophoneWireless Microphone/Pointer/White Board/* Equipped with neither Cable nor Wireless LANA beverage counter is available; please help yourself to the free drinks.Time availableBeverageAM9:00~ end of the lectureMineral water, Tea, Coffee, Green teaLibraryClosed AreaCommunityHallEntrance3. Room Seminar 1 :General Information / Late Registration(Dec 7 th (Wed)-9 th (Fri) )Secretariat is open throughout the conference according tothe Date and Time shown below.166 167

Outline Help counter: General information about the Conference.Photocopying, FAX transmissionsEquipment rentalTaxi callMedical emergenciesLost and found Travel counter: Staff from Kinki Nippon Tourist will assist you with your travel arrangement.Office hour Dec 6 th (Tue) PM2:00 ~ PM7:00Dec 7 th (Wed) AM9:00 ~ PM5:30Dec 8 th (Thu) AM9:00 ~ PM7:00Dec 9 th (Fri) AM9:00 ~ PM6:00BreakfastDate and Time5. Room 216 : Business BoothDec 7 th (Wed) - 9 th (Fri) AM9:00 ~ AM11:00Limited number of sandwich packs and beverage availablePlease feel free to use Room 216 for Internet connections,e-mailing, and so on. You can also use this room as your ownwork space.Free beverage is available. CloakYou can check in your luggage and coats.Office hourNoteDec 6 th (Tue) PM2:00 ~ PM8:40Dec 7 th (Wed) AM9:00 ~ PM5:30Dec 8 th (Thu) AM9:00 ~ PM8:40Dec 9 th (Fri) AM9:00 ~ PM6:00We recommend that you check in your luggage and coats asaisles are narrow and space is limited.4. Community Hall : Registration(Dec 6 th ) / Poster Presentation / DinningTime availableCapacityEquipmentAM9:00 ~ end of the lectureAbout 30 seatsCable LAN/ BeverageRegistrationDate and TimeNotePoster PresentationDisplaying PeriodLunchDinnerAll participants are required to register on Dec 6 th .Posters are displayed throughout the conference.Meals will be served in the Community Hall. Details areshown below.Dec 6 th (Tue) PM2:00 ~ PM3:00You can register at Room Seminar 1 after PM 3:30 on Dec6 th (Tue).Dec 6 th (Tue) PM3:00 ~ Dec 9th(Fri)PM5:30Poster Presentation Dec 8 th (Thu) PM5:00 ~ PM6:30Date and TimeDate and TimeDec 7 th (Wed) - 9 th (Fr)AM12:00 ~ PM2:00Buffet style/BeverageDec 6 th (Tue) & 8 th (Thu) PM6:30 ~ PM8:30Buffet style/Beverage6. EntranceTime schedules of the bus service to leave the IIAS for related hotels and stations are shown below.To Hotel Granvia KyotoDeparture-timeCapacityTo Kintetsu Shin-Hosono Station/JR Hosono StationDeparture-timeCapacityTo Keihanna PlazaHotelDeparture-timeCapacityPM 8:40 on Dec 6 th (Tue)PM 5:30 on Dec 7 th (Wed)PM 8:40 on Dec 8 th (Thu)PM 5:50 on Dec 9 th (Fri)About 40 ~ 50 seatsPM 8:45 on Dec 6 th (Tue)PM 5:35 on Dec 7 th (Wed)PM 8:45 on Dec 8 th (Thu)PM 5:55 on Dec 9 th (Fri)About 30 seatsPM 8:45 on Dec 6 th (Tue)PM 5:35 on Dec 7 th (Wed)PM 8:45 on Dec 8 th (Thu)PM 5:55 on Dec 9 th (Fri)About 30 seats168 169

Basic Philosophy and ObjectivesBasic Philosophy (Summary)We study ‘‘what we should study for the future and happiness of human beings.”Incorporation- August 22, 1984Authorized incorporation of the Foundation- October 1, 1993Opening of the InstituteThe International Institute for Advanced Studies (IIAS) was established as a foundation in 1984 with thestrong support of national and local governments, industrial sectors, and the academic community in Japan.Overview of Facilities- Total area:4ha, Total Floor Space : 6,000- Major Facilities:Administration building, community hall, research buildings A and B (library, seminar lounge, 2 seminarrooms, 26 research rooms, large research room, Japanese-style room, etc.), lecture hall (hall with about 120seats, and lounge)- Annexed Facilities:Director's residence, 6 family type houses, 1 single person apartment building consisting of 8 rooms, tea ceremonyroomThe land is loaned by Kyoto Prefecture free of charge. Construction funds for the facilities (including thegarden) were privately donated by the founder of OMRON Corporation, Mr. Kazuma Tateishi and his son Mr.Takao Tateishi, and assistance from Kintetsu Corporation was received. The tea ceremony room was donatedby Sen Genshitsu, Grand Master and the former head of Urasenke.The philosophy and objectives of the IIAS are to gather global wisdom, create and propose firm ideas asguidelines for the future of human beings generated and proposed by the Okuda Round Table in 1982, andthis spirit has been inherited continuously until now.How should we cope with the various issues that arise from the historical and social background in which welive? What should the proper posture be for culture, science and technology in the 21st century?The philosophy of the IIAS administration is that we should create new perspectives in academic world, aimto create new concepts, combine global wisdom, and contribute widely to the development of world culture bypursuing research on basic sciences and the humanities.ObjectivesThe objectives of the IIAS activity are to contribute to the development of novel advanced research fields andtopics, based on the close collaboration and exchange of first-class scientists and scholars from worldwide academia.ResearchPolicy for Research ProjectsThe International Institute for Advanced Studies offers the greatest features for providing forums for mutualunderstanding and close contacts among researchers in different academic disciplines. Based on this feature,the IIAS has the principal research objectives of excavating and developing new realms of sciences and the humanitiesfor the next generation by accumulation of knowledge in many academic fields through interaction ofoutstanding researchers.After reorganization of national universities and national research institutes as corporations, a significantlylarger ratio of research expenses is provided by competitive funding. Under the justification of promotion ofscience and technology, large research funding is granted to particular tasks and fields of national policies, andas a result, there is a growing tendency that researchers are concentrated in such particular tasks and fields.Considering the situation in which Japan is now placed, it is undoubtedly necessary to promote such problemsolving type research, but if too much focus continues to be placed on problem solving type research as weare witnessing now, while detailed knowledge can be accumulated in particular fields, such knowledge willeventually be depleted. This is because under such conditions, we cannot expect breakthroughs that createnew concepts and large scale developments in the sciences.In contrast, research based on the idea of individual researchers is problem excavation-type research, whichis basic academic study. In many cases, new tasks (new realms of sciences) of problem solving type researchemerges from the results and knowledge of problem excavation-type research. Therefore, it is necessary tomaintain a balance between problem solving type research and problem excavation-type research.Under such circumstances in Japan, our research projects have a great significance in that they could explore,discover and develop new realms of sciences for the next generation beyond even the boundaries ofnatural science and the humanities or social sciences. By providing a forum for discussion among outstandingresearchers both in Japan and overseas through our research projects and/or conferences, we want to transmitnot only research results and novel information to Japan and overseas but also to present to researchers andacademic societies, the possibility of development of sciences and important issues for the future of sciences.170 171

Research Planning CommitteeThe Research Planning Committee is comprised of the Director, Vice Directors and Academic Councilors(limited to 10 persons), which clarifies the basic idea and contents of the core research projects of the InternationalInstitute for Advanced Studies and promotes research projects under strong leadership.Main functions of the Committee are as follows.- Development of research projects and appointment of their principal investigators- Theme setting and appointment of organizers for IIAS Conferences- Investigation of trends in sciences and what research subjects should be taken into account and their prospects- Selection of members of Research Promotion Committee and Fellows, etc.- In addition, review of various tasks related to research activities of the IIAS according to referrals of the Directoror proposals to the DirectorResearch Promotion CommitteeResearch Promotion Committee is comprised of Vice Directors and outside prestigious experts in a varietyof fields (within 15 persons), which will put into practice the action plans of the matters determined by the ResearchPlanning Committee.Main functions of the Committee are as follows.- Assistance to Director and Vice Directors in relation to promotion of research projects and comprehensionand evaluation of the progress of research projects- Development of implementation plan of IIAS Conference- In addition, responses to various tasks related to research activities of the IIASWorking groups will be established from time to time whenever necessary for carrying out individual tasks.Contact9-3, Kizugawadai, Kizugawa city, Kyoto 619-0225 JAPANTEL: 81-774-73-4000FAX: 81-774-73-4005URL: http://www.iias.or.jp/en/E-mail: www_admin@iias.or.jp172